Clinical Application of Neuromuscular Techniques The Upper Body Volume 1

80 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 SC U LA R T E C H N I Q U E S : T H E U P P E R B O DY Hodges P, Heinjnen I, Gandevia S 2001 Postural activity of the Myers T 2001 Anatomy trains. Church.i ll Livingstone, Edinburgh d iaphragm is reduced in humans when respiratory demand Nixon P, Andrews J 1996 A study of anaerobic threshold i n chronic increases. Journal of Physiology 537(3):999-1008 fatigue syndrome (CFS). Biological Psychology 43(3):264 Hodges P, Eriksson A, Shirley D 2005 Intra-abdominal pressure Norris C 2000a The muscle debate. Journal of Bodywork and increases stiffness of the lumbar spine. Journal of Biomechanics 38(9 ) : 1 8 73-1880 Movement Therapies 4(4):232-235 Norris C 2000b Back stability. H uman Kinetics, Leeds Holmes T, Rahe R 1967 Social readjustment rating scale. Journal of O'Sullivan P, Beales D, Beetham J et al 2002 Altered motor control Psychosomatic Research 2:214 strategies in subjects w i th sacroiliac joint pain during the active Hubbard D 1993 Myofascial trigger points show spontaneous EMG straight-leg-raise test. Spine 27:E1-E8 activity. Spine 18:1 803-1807 Ost M, Van der Brink B, Rastinehad A et a l 2006 Hand pain d uring hand assisted laparoscopic nephrectomy - an ischemic event7 H urley M 1991 Isokinetic and isometric muscle strength and inhibi­ Journal of Urology 176(1):149-154 tion after elbow arthroplasty. Journal of Orthopedic Panjabi M 1992 The stabilizing system of the spine. Part 1. Function, Rheumatology 4:83-95 dysfunction, adaptation, and enhancement. Journal of Spinal Disorders 5:383-389 Janda V 1982 Introduction to functional pathology of the motor sys­ Peper E 2004 Repetitive strain computer user injury with biofeed­ tem. Proceedings of the VII Commonwealth and International back: assessment and training protocol. Online. Available: Conference on Sport. PhYSiotherapy in Sport 3:39 http : / / www.bfe.org/ protocol/ pro09eng.htm Peters D (ed) 2005 New medicine. Dorling Kindersl ey, London Janda V 1983 Muscle function testing. Butterworths, London Peters D, Chaitow L, Harris G, Morrison S 2002 Integrating Janda V 1988 Muscles and cervicogenic pain syndromes. In: Grant complementary therapies in primary care - a practical guide for health professionals. Churchill Livingstone, R (ed) Physical therapy in the cervical and thoracic spine. Edinburgh Churchil l Livingstone, New York Schlable H, Grubb B 1993 A fferent and spinal mechanisms of joint King J 1988 Hyperventilation - a therapist's point of view. Journal pain. Pain 55:5-54 of the Royal Society of Medicine 8 1 : 532-536 Selye H 1956 The stress of l i fe. McGraw-Hili, New York Knutson G 2005 Anatomic and flmctional leg-Iength inequality : a Shagss C, Malmo R 1954 Psychodynamic themes and localized review and recommendation for clinical decision-making. Part 1 . muscular tension during psychotherapy. Psychosomatic Anatomic leg-length inequa l i ty: prevalence, magnitude, effects Medicine 1 6(4):295-314 and clinical significance. Chiropractic and Osteopathy 1 3 : 1 1 Simons D 1993 Referred phenomena of myofascial trigger pOints. Kobassa S 1 9 8 3 Personal i ty and social resources i n stress resistance. In: Vecchlet L (ed) New trends in referred pain and hyperalgesia. Journal of Personal ity and Social Psychology 45:839-850 E lsevier, Amsterdam Korr I M 1978 Neurologic mechanisms in manipulative therapy. Simons D, Travel l J, Simons L 1999 Myofascial pain and dysfunc­ Plenum Press, New York, p 27 tion: the trigger point manual, vol l : upper ha lf of body, 2nd Larsson S E, Bodegard L, Henriksson K G, Oberg P A 1990 Chronic edn. Williams and Wilk ins, Baltimore tra pezius myalgia - morphology and blood flow studied in 17 Stedman's Electronic Medical Dictionary 2004 version 6.0. patients. Acta Orthopaed ica Scandinavica 6 l : 394-398 Lippincott Williams and Wilkins, Baltimore Latey P 1996 Feelings, muscles and movement. Journal of Timmons B 1994 Beha vioral and psychological approaches to Bodywork and Movement Therapies 1 ( 1 ) :44-52 breathing disorders. Plenum Press, New York Lederman E 1997 Fundamentals of manual therapy. Churchill TraveH J, Simons D 1992 Myofascial pain and dysfunction: the trig­ Livingstone, Edinburgh ger point manual, vol 2: the lower extremities. Williams and Lewis T 1942 Pain. Macmillan, New York Wi lkins, Ba ltimore Lewi t K 1985 Manipula tion in rehabi l itation of the locomotor sys­ Waersted M, Eken T, Westgaard R 1992 Single motor wlit activity in tem. Butterworths, London psychogenic trapezius muscle tension. Arbete och Halsa Liebenson C 1996 Rehab i l i ta tion of the spine. Williams and Wilkins, 17:319-321 Bal timore Waersted M, Eken T, Westgaard R 1993 Psychogenic motor Liebenson C 2006 Rehabilitation of the spine, 2nd edn. Lippincott uni t activity - a possible muscle injury mechanism studied Williams and Wilkins, Baltimore in a healthy subject. Journal of Musculoskeletal Pain Linton S 2000 Review of psychological risk factors in back and neck 1 (3 /4): 185-190 pain. Spine 25: 1 1 48-1156 WaUden M 2000 Lumbopelvic associations w i th hamstring strain in Lum L 1981 Hyperventilation - an anxiety state. Journal of the professional footballers. MSc Thesis, British College of Royal Society of Medicine 74:1-4 Osteopathic Medicine, London Maddi S, Kobassa S 1984 The hardy executive: health under stress. Win ters J, Crago P (eds) 2000 B iomechanics and neural control of Dow Jones-Irwin, Homewood, IL posture and movement. Springer, New York McConnell C 1962 Yea rbook. Osteopathic Institute of Appl ied Wittink H, Michel T 2002 Chronic pa i n management for physical Technique, Boulder, CO, p 75-78 thera pists, 2nd ed. B u tterworth-Heinemann, Boston McGill S M 1998 Low back exercises: prescrip tion for the healthy Wol fe F, Simons D 1992 Fibromyalgia and myofascial pain syn­ back and when recovering from inj ury. In: Resources manual for dromes. Journal of Rheumatology 19(6):944-951 guidelines for exercise testing and prescription, 3rd edn. Wolff H G 1948 Headache and other head pain. Oxford University American College of Sports Medicine, Indianapolis, IN. Williams Press, Oxford and Wilkins, Baltimore Wooten P 1996 Humor: an antidote for s tress. Holistic Nursing McGill S M, Sharratt M T, Seguin J 1995 Loads on spinal tissues Practice 10(2) :49-55 during simultaneous l i fting and ventilatory challenge. Ergonomics 38(9):1 772-1792 Mense S, Simons D, Russell I J 2001 Muscle pain: understanding its nature, diagnOSis, and treatment. 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81 Chapter 5 Patterns of dysfunction CHAPTER CONTENTS We have seen something of the interconnectedness of the structures of the body in Myers' fascial network model. A s Upper crossed syndrome 82 83 a consequence of the imposition of sustained or acute Lower crossed syndrome 82 stresses, adaptation takes place in the musculoskeletal sys­ tem and chain reactions of dysfunction emerge. These can Layer (stratification) syndrome be extremely useful indicators of the way adaptation has occurred and can often be 'read' by the c1i.nician in order to Chain reaction leading to facial and jaw pain: an help establish a therapeutic plan of action. example 84 When we observe, palpate and assess, in the many dif­ Patterns from habits of use 84 ferent ways that are outlined in this chapter (and the rest of The big picture and the local event 85 the book), we are operating in present time. Howevel� what Janda's 'primary and secondary' responses 85 is being revealed by such detective work relates to the com­ Recognizing dysfunctional patterns 86 pound culmination of past mechanical, chemical and emotional adaptations (stresses, strains, micro- and macro­ Excessive muscular tone 86 traumas, toxicities, deficiencies, fears, anxieties, somatizations and more) all overlaid on the unique, inborn idiosyncratic Simple functional tests for assessing excess muscular characteristics of the individual. tone 87 89 What is being looked at, touched, tested, pressed, stretched and evaluated is in the state it is because of everything that Functional screening sequence 88 has ever happened to it, and our task is to make sense of the evidence we can gather, to b uild a picture, to tell a story. Prone hip (leg) extension (PLE) test The evidence that emerges regarding the relative elasticity Trunk flexion test 90 of skin and fascia, the degree and na ture of shortness, Hip abduction test 90 strength, stamina and firing sequences of muscles, the Scapulohumeral rhythm test 91 changes in range of motion of joints, the presence or other­ Neck flexion test 92 wise of periosteal pain points, mechanical interference with Push-up test 92 nerves and myofascial trigger pOints, or the status of the indi­ Breathing pattern assessments 92 vidual's posture, brea thing and balance - all offer clues as to Seated assessment 92 the current level of adaptation and compensation. These (and Supine assessment 93 many other) palpable and assessable changes point us to the Sidelying assessment 93 processes that have taken, and are taking place, as the body Prone assessment 93 adapts to aging, gravity and the stresses of life. Trigger point chains 94 Just as an archaeologist patiently and painstakingly gath­ ers shards and slivers, and learns to interpret these frag­ ments of evidence from the past in order to construct a picture of what was, of what has been, so we must put together a coherent representation of why symptoms are as they are now, and what needs to be done to assist the indi­ vidual toward improvement or recovery.

82 CLINICAL A PPLICATION OF NEU ROMUSCULAR TEC HNIQUES: THE U P PE R BODY This involves ga thering evidence, and then interpreting Pectoralis major and minor which all tighten it in the context of the processes of which the individual is Upper trapezius and shorten currently part. How tight, loose, weak, bunched, flaccid, Levator scapulae symmetrical, balanced, sensitive or painful the tissues are Sternocleidomastoid all weaken can tell a potent story - but we have to add the words, the while explana tions. Lower and middle trapezius Serratus anterior and rhomboids Interpretation of the evidence emerges from the sensations that we perceive with our hands, and to which we add the As these changes take place they alter the relative posi­ descriptors that add color and pattern to the story. The thera­ tions of the head, neck and shoulders as follows. peutic choices that emerge from the patient's symptoms, his­ tory and the evidence that tests, palpation and assessment 1. The occiput and C1 and C2 will hyperextend, with the offer are a crucial part of the therapeutic encounter. head being translated anteriorly. There will be weakness of the deep neck flexors and increased tone in the suboc­ From the accumulated evidence we need to identify what cipital musculature. it is tha t the individual is adap ting to, the background to the presenting symptoms. Inappropria tely focusing on symp­ 2. The lower cervicals down to the 4th thoracic vertebra will toms ra ther than on trying to understand the bigger contex­ be posturally stressed as a result. tual picture, and then using this to frame stra tegies tha t encourage self-regulation, is likely t o retard recovery. 3. Rotation and abduction of the scapulae occur as the Intervention calls for therapeutic choices that reduce adap­ increased tone in the upper fixators of the shoulder (upper tive demands and /or enhance adaptive capacity - so allow­ trapezius and levator scapulae, for example) causes them ing self-regulation to operate more efficiently, while to become stressed and shorten, inhibiting the lower fixa­ simultaneously preventing exacerbations and recurrences. tors, such as serratus anterior and the lower trapezius. When a chain reaction develops, in which some muscles 4. As a result the scapula loses its stability and an al tered shorten (postural, type I) and others weaken (phasic, type direction of the axis of the glenoid fossa evolves, result­ II), predictable patterns involving imbalances emerge. Czech ing in humeral instability that involves additional leva tor researcher Vladimi r Janda MD ( 1982, 1 983) describes two of scapulae, upper trapezius and supraspinatus activity to these, the upper and lower crossed syndromes, as follows. maintain functional efficiency. UPPER CROSSED SYNDROME (FIG. 5.1) These changes lead to cervical segment strain, the evolution of trigger points in the stressed structures and referred pain The upper crossed syndrome, also known as the shoulder­ to the chest, shoulders and arms. Pain mimicking angina neck or proximal crossed syndrome (Liebenson 2006), may be noted, plus a decline in respiratory efficiency. involves the following basic imbalance. The solution, according to Janda, is to be able to identify the shortened structures and to release (stretch and relax) these, followed by reeducation toward more appropriate function. This key underlying pattern of dysfunction will be found to relate to a great many of the painful conditions of the neck, shoulder and arm, all of which will be considered in later chap ters. \\Nha tever other local trea tment these receive, consideration and reform of patterns, such as the upper crossed syndrome, must form a basis for long-term rehabilitation. INHIBITED TIGHT AND/OR SHORT LOWER CROSSED SYNDROME (FIG. 5.2) Deep neck flexors Trapezius and levator scapulae The lower crossed syndrome, also known as the hip-pelvic or distal crossed syndrome (Liebenson 2006), involves the following basic imbalance. TIGHT AND/OR SHORT INHIBITED Iliopsoas, rectus femoris which all tighten TFL, short adductors and shorten Pectorals Rhomboids and serratus anterior Erector spinae group of the trunk while all weaken Abdominal and gluteal muscles Figure 5.1 Upper crossed syndrome (after Janda). Reproduced with The result of this chain reaction is to tilt the pelvis for­ permission from Chaitow (1996). ward on the frontal plane, while flexing the hip joints and

5 Patterns of dysfunction 83 exaggerating lumbar lordosis. LS-Sl will have increased The solution for these common pa tterns is to identify both likelihood of soft tissue and joint distress, accompanied by the shortened and the weakened structures and to set about pain and irritation. An additional stress feature commonly normalizing their dysfunctional status. This might involve: appears in the sagittal plane in which: • deactivating trigger points within them or whi ch might Quadra tus lumborum shortens be influencing them while weaken Gluteus maximus and medius} • normalizing the short and weak muscles with the objec­ tive of restoring balance. This may involve purely soft tis­ When this 'lateral corset' becomes unstable the pelvis is sue approaches or be combined with osseous adjustment/ held in increased elevation and is accentuated when walk­ mobilization . ing. This instability results in LS-Sl stress in the sagittal plane, which leads to lower back pain. The combined Such approaches should coincide with reeducation of pos­ stresses described produce instability at the lumbodorsal ture and body usage, if results are to be other than short term. j unction, an unstable transition pOint at best. LAYER (STRATIFICATION) SYNDROME The piriformis muscles are also commonly involved. In (FIG. 5.3) 10--20% of individuals, the right piriformis is penetrated by either the peroneal portion of the sciatic nerve or, rarely, The layer (stratification) syndrome is a combination of upper by the whole nerve (the incidence of this is greatly increased and lower crossed syndromes. According to Janda et al in individuals of Asian descent) (Kuchera & Goodridge 1997). Piriformis syndrome can therefore produce direct sciatic pres­ Muscle hypotrophy Muscle hypertrophy sure and pain (but not beyond the knee) (Heinki ng et aI 1997). Lower stabilizers Cervical erector spinae Arterial involvement of piriformis shortness can produce of the scapula Upper trapezius ischemia of the lower ex tremity and, through a relative fix­ Levator scapulae ation of the sacrum, sacroiliac dysfunction and pain in the hip. Dural dysfunction is also possible when sacral mechan­ Thoracolumbar ics are distorted in this way as the deformations place ten­ erector spinae sion and torsion on the dural tube. An almost inevitable consequence of a lower crossed syndrome pattern is that stresses will translate superiorly, thereby triggering or aggrava ting the upper crossed syn­ drome pattern outlined above. We can once again see how the upper and lower body interact with each other, not only functionally but dysfunctionally as well. Lumbosacral erector spinae Gluteus maximus TIGHT AND/OR SHORT INHIBITED Hamstrings Erector spinae Abdominals INHIBITED TIGHT AND/OR SHORT Gluteus maximus Iliopsoas Figure 5.2 Lower crossed syndrome (after Janda). Reproduced with Figure 5.3 Layer (stratification) syndrome. Reproduced with permission from Chaitow (1996). permission from Juli Et Janda (1987).

84 CLINICAL A P PLICATION OF NEUROMUSCULAR TECHNIQUES: T HE U P PER BODY (2006), this has a poor prognosis for rehabilitation 'because assessed for the role they might be playing in the person's pain and restriction condi tions and certainly before these of the fixed muscle imbalance patterns at the central nerv­ can be successfully and appropriately treated. Various pro­ ous system level'. tocols will be ou tlined in later chap ters that can assist in this form of functional assessment. CHAIN REACTION LEADING TO FACIAL AND JAW PAIN: AN EXAMPLE PATTERNS FROM HABITS OF USE In case it is thought that such imbalances are of merely aca­ The influences in our da ily lives that relate directly to our demic interest, a practical example of the negative effects of habits of use in our work environment, homes and leisure the chain reactions described above is given by Janda activities greatly affect our musculoskeletal systems. The interaction between our bodies and the objects we are clos­ (1986). His premise is that TMJ problems and facial pain can est to (clothes, shoes, chairs, objects that we carry and with which we interact) can have profound influences on our be analyzed in relation to the person's whole posture. health, modifying the way we function, for good or ill. Janda has hypothesized that the muscular pa ttern associ­ As we go about our daily lives, we position ourselves to ated with TMJ problems may be considered as locally involv­ perform our work, to play sport, and even to sleep. These ing hyperactivity and tension in the temporal and masseter situations often involve repetitive and/ or prolonged stresses muscles while, because of this hypertonicity, reciprocal inhi­ that may lead to shortened, weakened, fibrotic or in other bition occurs in the suprahyoid, digastric and mylohyoid ways dysfunctional tissues. Consider also that these demands muscles. The external pterygoid, in particular, often develops are often placed on tissues that are already compromised by spasm. previous traumas or habits of use. This imbalance between 'jaw adductors' (mandibular For example, consider the person who has recently eleva tors) and 'jaw openers' (mandibular depressors) alters acquired a job that demands a lot of time spent on the tele­ the ideal position of the condyle and leads to a consequent phone while simul taneously using their hands on the com­ redistribu tion of stress on the joint while contributing to pu ter. The job is set in an open environment where the use degenerative changes. of a speaker phone compromises privacy, so she tends to hold the phone with her shoulder while typing with her Janda describes a typica l pattern of muscular dysfunc­ hands. The elevation of the shoulder shortens levator scapula tion of an individual with TMJ problems as i nvolving upper and upper trapezius while side flexion of the neck affects the trapezius, levator scapulae, scalenii, sternocleidomastoid, scalene muscle group. Even with the addition of a shoulder suprahyoid, lateral and medial pterygoid, masseter and pad to the phone, the habit of holding the phone wedged in temporalis muscles, all of which show a tendency to tighten this manner on a frequent, daily basis will lead to changes and to develop spasm. He notes that while the scalenes are in the tissues that are being used. However, the problem can unpredictable, commonly when overloaded, they will cascade further. become atrophied and weak and may also develop spasm, tenderness and trigger points. As the tissues become chronically tight and her head changes position due to lateral flexion (with mandatory The postural pattern associated with TMJ dysfunction rotation) of the cervical vertebrae, her center of gravity is might therefore involve: affected. To remedy this, her body must adapt to the offset head position by counterbalancing, a task that is easily 1. hyperextension of the knee joints achieved by a tightening of the contralateral quadratus 2. increased anterior tilt of the pelvis lumborum (or erector spinae or any number of other mus­ 3. pronounced flexion of the hip joints cles). As this adaptation occurs, a cascade of other changes 4. hyperlordosis of the lumbar spine may erupt, including tightening of adductors, hamstrings 5. rounded shoulders and winged (rotated and abducted) and/ or gastrocnemius, and even foot pronation (Joss of plantar vault integri ty) . This, in turn, can affect gait and the scapulae ability to deal with ground force reactions as they travel 6. cervical hyperlordosis back up through the body with every step taken. 7. forward head pOSition Remedies to problems deriving from this sort of back­ 8. compensatory overactivity of the upper trapezius and ground of overuse, misuse and abuse of the body are obvi­ ous, and might involve either completely avoiding, or at levator scapulae muscles least changing, the pattern of use (for example, acquiring a headset for the telephone) or performing activi ties to help 9. forward head position resulting in opening of the mouth counterbalance the negative effects of the behavior in ques­ tion (stretching, toning, exercising, etc.) . and retraction of the mandible. This series of changes provokes increased activity of the jaw adductor (mandibular elevator) and protractor muscles, cre­ a ting a vicious cycle of dysfunctional activity. Intervertebral join t stress in the cervical spine follows. The message which can be drawn from this example is tha t patterns first need to be identified before they can be

5 Patterns of dysfunction 85 Treatment of patterns of imbalance that result from trauma, • muscle spasm or from habitually stressful patterns of use, needs to address • and a sequence of events which would then include com­ the causes of residual pain, as well as a im to improve these patterns of voluntary use, with a focus on rehabilitation pensation and adapta tion responses in many muscles, toward normal proprioceptive function. In Volume 2 of this followed by the evolution of a variety of possible syn­ textbook, some of the important influences of the close envi­ dromes involving head/neck, TMJ, shoulder/arm or ronment and habits of use are discussed and perspectives others. emerge that will encourage practitioners to use their own bodies more efficien tly and less stressfully, as well as being Janda's point is that after all the adapta tion that has taken able to advise and guide their recovering patients appropri­ place, treatment of the most obvious cervical restrictions, ately regarding the everyday influences of their close envi­ where the person might be aware of pain and restriction, ronments. Active, dynamic rehabilitation processes tha t would offer limited benefit. He points to the existence of reeducate the individual and enhance neurological organi­ oculopelvic and pelviocular reflexes, which indicate tha t zation may usefully be a ssisted by passive manual meth­ any change in pelvic orienta tion alters the position o f the ods, including basic massage methodology and soft tissue eyes and vice versa, and to the fact tha t eye position modi­ approaches as ou tlined in these textbooks. fies muscle tone, pa rticularly the suboccipital muscles (look up and extensors tighten, look down and flexors prepare for THE BIG PICT URE AND THE LOCA L EVENT activity, etc.). The implica tions of modified eye position due to altered pelvic position therefore become yet another fac­ As adaptive changes take place in the musculoskeletal sys­ tor to be considered when unraveling chain reactions of tem and as decompensa tion progresses toward an inevitably interacti.ng elements (Komendantov 1945). These examples,' more compromised degree of function, structural modifica­ Janda says, 'serve to emphasize that one should not limit tions become evident. Whole body, regional and local pos­ consideration to local clinical symptomatology . . . but [that tural changes, such as those described by Janda (crossed we] should always maintain a general view.' syndromes) and epitomized in the case of facial pain out­ lined above, commonly result. Grieve (1986) echoes this viewpoint. He explains how a Simultaneously, with gross compensatory changes mani­ patient presenting with pain, loss of functional movement festing as structural distortion, local influences are noted in or a ltered pat terns of strength, power or endurance will the soft tissues and the neural reporting stations situated probably either have suffered a major trauma, which has within them, most notably in the proprioceptors and the overwhelmed the physiological limits of relatively healthy nociceptors. These adaptive modifications include the tissues, or will be displayi.ng 'gradual decom pensa tion phenomenon of facilitation and the evolution of reflexo­ demonstrating slow exhaustion of the tissue's adaptive genically active structures in the myofascia (detailed in potential, with or without tra uma' . As this process of decompensation occurs, progressive postural adapta tion, Chapter 6). influenced by time factors and possibly by trauma, leads to exhaustion of the body's adaptive potential and results in JANDA'S 'PRIMARY AND SECONDARY' dysfunction and, ultimately, symptoms. RESPONSES Cholewicki & Silfies (2005) remind us of Hooke's law, It has become a truism that we need to consider the body as which states tha t within the elastic limits of any substance, a whole; however, local focus still seems to be the dominant the ratio of the stress applied to the strain produced is in rela tion to the force constant. Hooke's law describes the clinical approach. Janda (1988) gives various additional relation of tension and ex tension w i thin an object's elastic limits. When we apply a tension on an object, it will be elon­ examples of why this is extremely shortsighted. He dis­ gated in relation to the force constant, i.e. the stiffness of its cusses the events that follow on from the presence of a short spring qua lity. However, if it is subjected to a very large ten­ leg, which might well include: sion, its extension will not be proportionate to the applied tension. The maximum tension for it to obey Hooke's law is • al tered pelvic position called the elastic limit. Beyond that, it will break or fail to • scoliosis fully recoil. This is true for connective tissue, both in trauma • probable joint dysfunction, particularly at the cervicocra­ and in therapy nial junction In simple terms, this means tha t tissue capable of defor­ • compensatory activity of the small cervicooccipital mation will absorb or adap t to forces applied to it within its muscles The stress applied to stretch or compress a body is proportional to • modified head position the strain or change in length thus produced, so long as the limit • later compensation of neck musculature of elasticity of the body is not exceeded. • increased muscle tone

86 CLINICAL A PPLICATION OF NEU ROMUSCULAR TECHNIQUES: THE U P PE R BODY elastic limits, beyond which it will break down or fail to narmal aI', in same cases, nat at all. Hence the arder in which compensate (leading to decompensation). Grieve rightly muscles cantract is altered, as is caardinatian. The mast reminds us that while attention to specific tissues incrimi­ characteristic feature, hawever, is substitutian, altering the nated in producing symptoms often gives excellent short­ entire pattern. This change is particularly evident if the term results, 'Unless treatment is also focused toward weak muscle is the aganist. If, hawever, the neutralizers restoring function in asymptomatic tissues responsible for and/ar fixatars are weak, the basic pattern persists but there the original postural adapta tion and subsequent decom­ is accessary matian; ifthe antagonists are weak, the range of pensation, the symptoms will recur'. matian is increased. (Vasilyeva & Lewit 1996) RECOGNIZING DYSF UNCTIONA L PATTERNS An example of Vasilyeva & Lewit's findings, relating specif­ ically to a shortened upper trapezius, includes the follow­ Vasilyeva & Lewit (1996) have cataloged observable changes ing observations. in m uscle, elevating the art of inspection to a higher level. With a short upper trapezius muscle the a ttachments will They state: deviate as follows, causing the listed changes. Because muscular imbalances manifest in individual mus­ • The occipital bone will be pulled caudoventrally and cles and therefore (primarily) in certain regions, but are fol­ slightly laterally, causing the head to deviate forward lowed by compensatory reactions in other areas that restore and to the side, with rotation to the opposite side, leading balance, it is most important to determine which muscle(s) to craniocervical lordosis. and which region are primarily affected and where compen­ sation is taking place. • There will be pull on the spinous processes adding to sidebending and rotation to the opposite side. In com­ Among the main criteria examined when assessing for pat­ pensation, scoliosis will develop at the cervicothoracic terns of imbala nce, for example in an extremity joint, are the j unction, to the ipsilateral side, with increased kyphosis. following. • There will be relative fixation of the cervical and upper • Can the movement be carried out in the desired direction? thoracic spine with increased mobility at the craniocervi­ • Is the movement smooth and of constant speed? cal and cervicothoracic junctions. • Does the movement follow the shortest path? • Does the movement involve the full range? • The acromion will be pulled craniomedially, leading to the clavicle and acromion devia ting craniomedially, pro­ The decision as to which muscles are probably implicated ducing compression of the clavicle at the sternal articula­ when abnormal responses are noted is based on the tion, with compensation involving sidebending at the following. shoulder girdle toward the opposite side, with rota tion to the ipsila teral side. • Dysfunction of agonists and synergists when the direc­ tion of movement is abnormal. The motor patterns during shoulder abduction, which will be disturbed with a shortened upper trapezius, include the • Neutralizer muscles are implicated if precise motion is following. missing. • There will be a shearing between the clavicle and scapula • If movement is other than smooth, antagonists are at the acromioclavicular joint. implicated. • The head and cervical spine w ill move into extension, Wha t happens if the main culprits in disturbed motor pat­ ipsilateral flexion and contralateral rotation. terns are shortened muscles? • The shoulder girdle will displace superiorly on tha t side. The shortened muscle is also hyperactive as a rule. Its irrita­ tion threshold is lowered and therefore it contracts sooner Observation may also alert the practitioner to the presence than normal, i.e. the order in which muscles contract in the of a crossed syndrome - pelvis tilted anteriorly, protruding normal pattern is altered. If, therefare, the aganist is shart­ abdomen, increased thoracic kyphosis, head thrust for­ ened, the relationship to' the synergists, neutralizers, fixa­ ward, rounded shoulders, etc. But which muscles, specifi­ tars and antaganists is aut af balance and the lacal pattern, cally, among the many involved, are demonstrating relative i.e. the direction, smoothness, speed and range af matian, is shortness or weakness or both? Testing is needed and this disturbed in a characteristic way. (Vasilyeva & Lewit 1996) can involve functional tests (below), as well as a ssessment of length and strength. A munber of these tests will be What happens if the main culprits in disturbed motor pat­ detailed in the text a ssociated with particular regions and terns are weak muscles? joints later in the book. The threshold of irritation in the weakened muscle is raised EXCESSIVE MUSCULAR TONE and therefare, as a rule, the muscle cantracts later than Muscle tone (residual muscle tension) is the continuous, passive partial contraction of muscles. It helps maintain

5 Patterns of dysfunction 87 posture and is often even present during REM sleep. It • The limitation of range of motion of a muscle is estimated depends physiologically on two factors: the basic viscoelastic clinicaUy by slowly extending the muscle until it reaches properties of the connective tissues associated with the mus­ a barrier of increasing tension, which could be because of cle and/or the degree of activation of the contractile appara­ increased viscoelastic tension, spastici ty, physiological tus of the muscle Oanda et a12006, Simons & Mense 1 998). con tracture or fibrosis. vVhen this test shows increased range of motion (hypermobility) it suggests decreased Janda et al (2006) discuss the importance yet difficulties muscle tone or laxity of ligamentous and capsular con­ of differen tial diagnosis since each condi tion requires a dif­ nective tissues. ferent type of treatment: • A 'flapping test' for assessing hypo- and hypertonia is In the former [viscoelastic properties], we speak about muscle performed by 'grasping the fingertips of the extended tightness, stiffness, loss offlexibility or extensibility (length) arms and rhythmically shaking them up and down to see and in the latter [contractile properties], it is a real increase how loose or how stiff the musculature of each extremity of muscle contractile activity such as in spasmodic torticol­ is'. With progressively more rapid movements, the exam­ lis or trismus . . . Clinically, resting muscle tone presents a iner can estimate the resonant frequency of each limb. combination of both situations (contractile and viscoelastic Proximal-distal and bilateral differences are noted. properties) . . . However, measuring muscle tone objectively presents a dilemma. Tests of viscoelasticity involve measure­ • The Wartenberg pendulum test: This simple but extremely ments of the velocity of motion, viscosity, thixotropy, and useful test is performed with the relaxed patient sitting resonantfrequency when load is gradually applied. Tests of on the edge of the table with legs hanging freely over the contractile activity are far simpler in tlUlt EMG can be used; edge. The examiner lifts both legs to the horizontal posi­ however, this is not without inherent difficulties, as in trig­ tion (knees straight) and then releases them, observing ger points where only small loci in the muscle show their movement as they swing freely. A normal leg increased electrical activity. The degree of muscle stiffness swings in smoothly decreasing arcs. However, overreac­ in relaxed subjects can be seen therefore to include both vis­ tive reflex activity reduces the number and smoothness coelastic tone and muscular contractile factors. of oscillations of an affected limb, while muscular hypo­ tonia gradually decreases the amplitude of the arcs. Regardless of the source, excessive muscular tone is undesir­ able since it interferes with normal physiological function­ Hannon (2006) has revisited this simple test which was ini­ ing as well as being wasteful of energy. Yet, it is important to tially developed in the early 1 950s by Wartenberg (1951). differentiate - through palpa tion of the layers of tissue Hannon suggests tha t this test can be used to evaluate exces­ (skin, fascia, fat, muscle fibers, etc.) and inspection of pos­ sive, Lmnecessary tension in the quadriceps, which offers ture, patterns of movement and gait analysis - as much as is evidence of what he terms 'underlying \"parasitic\" muscular subjectively and objectively possible to determine as the effort' tha t represents a current inability for the individual cause for the increased tone. to relax the muscles involved. Hannon notes tha t patellar tension is often seen in the asymptomatic individual, and, SIMPLE FUI\\ICTIONAL TESTS FOR ASSESSING in fact, 'it is rare to find adults able to fully relax the patella EXCESS MUSCULAR TONE at will'. Simons & Mense (1 998) define resting muscle tone as the • The patient is in a Sitting position with the legs hanging vertically. 'elastic and/or viscoelastic stiffness ianntdh/e oarbsceonnctreaoc tfucroen),­. tractile a c ti v i t y (motor unit activity • The leg under examination is passively ex tended to 45° and then released. Lakie et al (1980) concluded tha t there was no reduction in • The pendular movement of the leg is observed and tone as a resu lt of surgical anesthesia and therefore tha t the documented. elastic tone of normal resting muscle must be caused by i ts • In a relaxed state approximately 10 cycles of elliptical pendulum swings will occur. 'The classic observation is viscoelastic properties in the a bsence of muscle contractile the number of cycles accrued before the leg comes to rest.' activity. In clinical practice muscle tone is measurable as This simple test has been applied to the study of aging mus­ cle responsiveness, cerebral palsy, fibromyalgia, spinal cord stiffness, which is the resistance to passive movement. injury and vertebral conditions (Fowler et al 2001, Le Cavorzin et al 200 1 , Wachter et aI1 996). Studies in 1998 (Simons & Mense) and 2001 (Mense & Hann on notes that even Simons) led the authors to suggest the following simple excess muscular effort since tension in the hip rota tors turns the femur either internally or externally. This deviates the methods for evaluating muscle ' tone': shin from the vertical in the frontal plane. The trajectory of the foot during the oscilla tion of the swinging knee, shin pos­ • The compliance (compressibility) of a muscle is assessed ture and extraneous effort all offer additional informa tion. clinically by pressing a finger into it or by squeezing i t between the fingers to determine how easily i t i s indented and how 'springy' it is. The less easily it is indented, and the more it tends to return to i ts original shape, the more stiff (elastic) it is.

88 CLINICAL A P PLICATION OF NEUROMUSCULAR TEC HNIQUES : THE U P PER BODY \" ,I , ,, II I II �, I I \\ I \\ I \\ \\ \\ \\, ... � A B (i) (ii) c Figure 5.4 A: Wartenberg pendulum test. Sitting, the patient's leg is extended to 45°. The leg is released and the pendular swing is observed and documented. B: Resting shin position. Observation of resting shin posture may identify subtle muscle tension. A slanted shin in the frontal plane suggests hip rotator tension. A sagittal slant points toward tension in the knee flexors or extensors. C: Extraneous exertion and passive knee movements. The knee is moved passively to help the patient notice extraneous effort. At fi rst, use only the smallest of movements. Watch for shudderi ng and stiffness. D: Elliptical versus l inear foot trajectory. In the picture, the shin appears l i ke a swinging shaft hanging from a hook. If the hook also rolls, as does the femur, the freely moving shin w i l l reflect both the swinging and ro l l i ng movements. Relaxed pelvic rotators, hamstrings and quadriceps muscles allow the swinging foot to travel an ell iptical path. Tensing the hip rotators restricts travel to a linear trajectory. Tensing the other muscles reduces the extent of the swing. Reproduced with permission from Hannon (2006). Janda has developed a series of assessments - functional A key aspect of Janda's functional assessments relates to tests - that can be used to show changes that suggest imbal­ the proposed firing sequence of muscles when particular ance, via evidence of over- or underactivity. Some of these actions (e.g. hip ex tension, hip abduction) are performed. are outlined below. Jull & Janda (1987) observed that the firing order of the F UNCTIONAL SCREENING SEQ UENCE key muscles for hip/ leg ex tension should be as follows: first the ipsilateral hamstrings, followed by ipsilateral glu teus Janda (1996) and Janda et al (2006) have claimed that altered maximus, and then contrala teral lumbosacral erector movement patterns can be tested as part of a screening spinae, ipsila teral lumbosacral erector spinae, contralateral examina tion for locomotor dysfunction. In general, obser­ thoracolumbar erector spinae and finally ipsila teral thora­ vation a lone is said to be all that is needed to determine columbar erector spinae. the al tered movement pattern. However, light palpation may also be used if observa tion is difficult due to poor light­ Janda (1982) described the hamstrings and gluteus max­ ing, a visual problem or if the person is not sufficiently imus as prime movers in prone hip extension, with the erec­ disrobed. tor spinae stabilizing the spine and pelvis. Although some of these tests relate directly to the lower Based on EMG studies, Vogt & Banzer (1997) disagreed, back and limb, their relevance to the upper regions of the and suggested that the firing pa ttern for prone hip exten­ body should be clear, based on the interconnectedness of sion should be: ipsilateral erector spinae, followed by ipsi­ body mechanics, as previously discussed. lateral hamstring, contrala teral erector spinae, tensor fascia latae and finally gluteus maximus. The usefulness and accuracy of some of these tests has been brought into question by research that shows inconsistency

5 Patterns of dysfunction 89 Figure 5.5 Hip extension test as described in text. Reproduced with permission from Chaitow (1996). in some of the purported firing patterns (see description In the test (below) it is suggested that both the movement below), when groups of asymptomatic individuals were pattern, as well as the timing sequence, should be observed. tested. The question is also raised as to how accurate palpa­ tion methods can be when the difference in firing between PRONE HIP (LEG ) EXTENSION (PLE) TEST specific muscles may be as little as 30 milliseconds (Lehman (FIG. 5.5) et aI2004). Purpose: To assess for the presence of true or false hip exten­ The answer to at least some of the objections involves a sion, as well as to check for coordinated firing pa tterns dur­ weakness in the research in which asymp tomatic individuals ing hip extension. Janda did not encourage the palpation are the subjects used in the studies. This factor alone ensures approach described below be performed simultaneously that the population being studied fails to match pa tients with the observations, and suggested that it interfered with who will be seen clinically - who by definition are unlikely normal function. Instead he encouraged observation first, to be asymptomatic. as described, and suggested tha t ii palpation is carried out during the test, this should be after first evalua ting the Lehman et al note that 'In this current study the only con­ movement pa tterns by observation alone. sistent finding between subjects was tha t 13/14 subjects fired the gluteus maximus last [on prone leg extension].' Observation with palpation In Janda's observation, this finding would be most likely • The person lies prone and the practitioner stands to the to occur when gluteus maximus is inhibited, probably due side at waist level with the cephalad hand spanning the to excessive tone/ activity in the erector spinae group. Since lower lumbar musculature and assessing erector spinae this is a very common clinical presenta tion in symptomatic activi ty bila terally. individuals, it is reasonable to assume tha t many asympto­ matic individuals have similar imbalances prior to the onset • The caudad hand is placed so that the heel lies on the of symptoms. This is acknowledged by the researchers gluteal muscle mass with the fingertips on the hamstrings. who state: • The person is asked to raise the leg into extension as the [We were] unable to identify what is truly an abnormal pat­ practi tioner assesses the firing sequence. tern of muscular activation. While the participants included in this study had no current symptoms they may still have • The normal activation sequence is said to be (1) gluteus dysfunctional motor activation patterns, which have not maximus, (2) hamstrings, followed by (3) erector spinae presented symptomatically. Future studies should look at contrala teraL then (4) ipsilatera l. (Note: As discussed the relationship between activation patterns and the onset of above, not all researchers or clinicians agree with this future dysfunction. It should also be noted that the PLE test sequence. Some believe the hamstrings should fire first, is also used to assess the movement kinematics of patients. or that there should be a simultaneous contraction of This paper only investigated muscle onset timing and did hamstrings and gluteus maximus.) not assess movement kinematics. The PLE test may still be a valid test for assessing movement dysfunction, however, • If the hamstrings and / or erectors take on the role of no work has been done to assess this possibility. glu teus as the prime mover, they w ill become shortened

90 CLINICAL A P PLICATION OF NEUROMUSCULAR TECHNIQUES: THE U P PER BODY (see notes on postural and phasic muscle response to TRUNK FLEXION TEST (FIG. 5.6) stress and overuse in Chapter 2). • Janda says, 'The poorest pattern occurs when the erector • The person is supine with arms extended and reaching spinae on the ipsilateral side, or even the shoulder girdle toward the knees, which are flexed with feet flat on table. muscles, initiate the movement and activation of gluteus maximus is weak and substantially delayed . . . the leg lift • The person is asked to maintain the lumbar spine against is achieved by pelvic forward tilt and hyperlordosis of the table and to slowly lift the head, then the shoulders the lumbar spine, which undoubtedly stresses th.is and then the shoulder blades from the table. region' . • Normal function is represented by the ability to raise the Kinesthetic aspect of the test trunk until the scapulae are clear of the table without the feet lifting or the lower back arching. • When the hip extension movement is performed there should be a sense of the lower limb 'hinging' from the hip • Abnormal function is indicated when the feet (or a foot) j oint. lift from the table or the low back arches, before the scapulae are raised from the table. This indicates psoas • If, instead, the hinge seems to occur in the lumbar spine, overactivity and weakness of the abdominals. the indication is tha t the lumbar spinal extensors have adopted much of the role of gluteus maximus and that Note: It may be helpful for the practitioner to slide his hand these extensors (and probably hamstrings) will have under the patient's lower back prior to testing to directly shortened. feel the lifting of the lumbar spine since this movement may not be readily visible on some patients. Morris et al (2006) observe tha t the test is positive (i.e. the pattern is dysfunctional) if: HIP ABDUCTION TEST (FIG. 5.7) 1. significant knee flexion of the ipsilateral leg occurs, sug­ Purpose: To screen for the dynamic stability or instability of gesting overactiva tion of the hamstrings the lumbopelvic region during hip abduction. • The person lies on the side, ideally with head on a cush­ 2. there is delayed or absent ipsilateral gluteus maximus contraction. Th.is is considered a very important finding ion, with the upper leg straight and the lower leg flexed 3. the presence of false hip extension is observed. This is ------ demonstrated when the pivot point (hinge) of the leg extension during the initial 10° occurs totally or in part a t Figure 5.6 Trunk flexion test. If feet leave the surface or back the sacroiliac region, instead of totally at the hip joint arches, psoas shortness is indicated. Reproduced with permission from ehaitow (1996). 4. lowering of the flank occurs on either side, suggesting rotation due to poor lumbopelvic functional stability 5. early contraction takes place at the periscapular muscu­ lature, strongly suggesting a chronic functional low back instability. This is most frequently observed on the con­ tralateral side. This finding suggests that recruitment of the upper torso muscula ture has occurred during the hip extension movement pattern in order to expedite the process. Figure 5.7 Hip abduction test which, if normal, occurs without 'hip hike' (A), hip flexion ( B) or external rotation (el. Reproduced with permission from ehaitow (1996).

5 Patterns of dysfunction 9 1 at hip and knee, for balance. The uppermost (straight) leg • The person is asked to let the arm being tested hang should rest on the lower leg, the hip of which should be down and to flex the elbow to 90° with the thumb point­ flexed to 45° while knee should be flexed to 60°. It is ing upward. important for the patient's upper leg to remain in line with the torso. • The person is asked to slowly abduct the arm toward the • The practitioner, who is observing, not palpating, stands horizontal. in front of the person and toward the head end of the table. • The person is asked to slowly raise the leg into abduction. • A normal abduction will include elevation of the shoul­ • Normal is represented by pure hip abduction to 45°. Note: der and/ or rotation or superior movement of the scapula The leg should abduct to 20° withou t in ternal or external only after 60° of abduction. rotation or any hip flexion. There should be no ipsilateral pelvic 'hip hike' (cephalad elevation). A slight initial con­ • Abnormal performance of this test occurs if elevation of traction of the lumbar erector spinae or quadratus lum­ the shoulder, rotation, superior movement or winging of borum may be observed. This is considered to represent a the scapula occurs within the first 60° of shoulder abduc­ normal isometric stabilizing contraction . tion, indicating levator and/or upper trapezius as being • Abnormal is represented by: overactive and shortened, while lower and middle trapez­ 1. hip flexion during abduction, indicating tensor fascia ius and serra tus anterior are inhibited and are therefore weak. lata (TFL) shortness, and/or 2. the thigh externally rotating during abduction, indi­ Variation 1 ca ting piriformis shortness, and/ or • The person performs the abduction of the arm as described 3. 'hip hiking', indicating quadratus lumborum short­ above and the practitioner observes from behind. ness (and probable gluteus medius weakness), and/ or • A 'hinging' should be seen to take place at the shoulder 4. posterior pelvic rotation, suggesting short antagonis­ joint, if upper trapezius and levator are normal. tic hip adductors. Variation 1 A • Before the test is performed the practitioner (standing behind the sidelying patient) lightly places the fingertips of the cephalad hand onto the lateral margin of quadratus lumborum while also placing the caudad hand so that the heel is on gluteus medius and the fingertips on TFL. • If quadratus lumborum is overactive (and, by definition, shortened - see p. 34), it will fire before gluteus and pos­ sibly before TFL. • The indication would be that quadratus (and possibly TFL) had shortened and that gluteus medius was inhib­ i ted and weak. Variation 2 • When observing the abduction of the hip, there should be a sense of 'hinging' occurring at the hip and not at waist level. • If there is a definite sense of the hinge being in the low back/waist area the implication is the same as in varia­ tion 1 - that quadra tus is overactive and shortened, while glu teus medius is inhibited and weak. ,. SCAPULOHUMERAL R HYTHM TEST (FIG. 5.8) B This test has direct implications for neck and shoulder Figure 5.8 Scapulohumeral rhythm test. A : Normal. B: Imbalance dysfunction. due to elevatio n of the shoulder within first 60° of abduction. Reproduced with perm ission from Chaitow ( 1 996). • The person is seated and the practitioner stands behind to observe.

92 CLINICAL A P P LICATION O F NEUROMUSCULAR TECHNIQUES : THE U PPER BODY • If 'hinging' appears to be occurring at the base of the PUSH - U P TEST neck, this is an indication of excessive activity in the upper fixators of the shoulder and shortness of upper trapezius • The person is asked to perform a push-up and /or to lower and / or levator scapula is suggested. himself from a push-up position, as the practitioner observes scapulae behavior. Variation 2 • A normal result will be evidenced by the scapulae pro­ • The person is seated or standing with the practi tioner tracting (moving toward the spine) without winging or standing behind with a fingertip resting on the mid-por­ shifting superiorly as the trunk is lowered . tion of the upper trapezius muscle of the side to be tested. • If the scapulae wing, shift superiorly or rotate, the indi­ • The person is asked to take the arm into extension (a cation is tha t the lower stabilizers of the scapulae are movement which should not involve upper trapezius). weak (serratus anterior, upper and middle trapezius). • If there is discernible firing of upper trapezius during In addition to these 'snapshot' pictures of functional imbal­ this movement of the arm, upper trapezius is overactive ance tha t offer strong indica tions of which muscles might and, by implication, shortened. individually be short and/ or weak, a range of tests exists for individual muscles. Some of these will be detailed in the N ECK FLEXION TEST (FIG. 5.9) appropriate sections of the therapeutic applications section of the book. • The person is supine without a pillow. • The person is asked to lift the head and place the chin BREAT HING PATTERN ASSESSMENTS on the chest while raising the head no more than 2 cm Motor control is a key component in spinal (and all joint) from the table. injury prevention, and loss of motor control involves failure • A normal result occurs if there is an ability to hold the to control joints, commonly because of poor coordination of chin tucked in while flexing the head/ neck. the agonist-antagonist muscle coactivation. • Abnormal is represented by the chin poking forward during this movement, which indicates sternocleidomas­ Three subsystems work together to maintain spinal sta­ toid shortness and weak deep neck flexors. bility (Panjabi 1 992): ( • central nervous subsystem (control) • osteoligamentous subsystem (passive) ( • muscle subsystem (active). A There is evidence tha t the effects of breathing pattern disor­ ders, such as hyperventilation, result in a variety of nega­ \"­ \" I tive influences and interferences, capable of modifying each of these three subsystems (Chaitow 2004, Hamaoui et al \\ 2002). B ------ The following tests assess the patient's breathing pat­ terns. It is suggested that the practi tioner observe several Figure 5.9 N eck flexion test. A: Normal flexion. B: Abnormal flexion breathing cycles with each test. ('chin poking' ) . sugges ting shortness of SCM. Reproduced with SEATED ASSESSMENT (J a n d a 1 9 8 2 ) permission from Chaitow ( 1 996). 1. The patient places a hand on the upper abdomen and another on the upper chest. The practitioner observes the hands as the pa tient inhales and exhales normally several times. If the upper hand (chest) moves superiorly rather than anteriorly, and moves significantly more than the hand on the abdomen, this suggests a dysfunctional 'upper chest' pattern of brea thing (see Fig. 14. 1 0, p. 553). 2. The practitioner stands behind and places both hands gently over the upper trapezius area, fingertips resting on the superior aspect of the clavicles. As the patient inhales the practitioner notes whether the hands move significantly superiorly. If they do, the scalenes are overworking, indicating stress and therefore possible shortening.

5 Patterns of dysfunction 93 3. The practi tioner stands or crouches facing the pa tient the lower rib cage, fingers wrapping posteriorly along who is seated on the edge of the treatment table and the rib shafts. The tissues are then tested for their rota­ places the hands on the patient's lower ribs, one on each tional preference, by easing the superficial tissues and side with fingers wrapping to the posterior surface, and the ribs in a rotational manner, right and then left. Ideally, notes whether there is lateral excursion of the hands on a symmetrical degree of rota tion should be noted. inhala tion to evaluate symmetry of movemen t. SID ELYING ASSESSME NT 4. Standing to the side the practitioner observes the spinal contours as the patient fully flexes. If there a re obvious Quadratus lumborum is tested for shortness by direct pal­ 'flat' a reas of the spine (suggesting inability to flex fully), pation (see Volume 2) and/or by use of the functional especially in the thoracic region, this may indicate rib assessment described earlier in this chap ter. Quadratus restrictions at those levels. lumborum is connected to the diaphragm (via a fascial encasement tha t becomes the lateral arcuate ligament) SUPI NE ASSESSMENT (Palastanga et al 2002) as weJ l as to the 12th rib (via d irect attachmen t). QL may be involved in breathing dysfunction, 1 . The brea thing pattern is observed. Does the abdomen particularly when there is reduced lower rib excursion. move forward on inhala tion, or does the upper chest inappropriately move first while the abdomen retracts? If PRONE ASSESSMENT the latter, breathing retraining is called for, as this is a paradoxical breathing pattern. 1 . The so-called 'breathing wave' is observed - there should be a continuous wave from the base of the spine to the 2. Is there a normal observable lateral excursion of lower ribs? neck on deep inhalation (Lewit 1 999). If movement starts 3. Assessmen t should be performed for shortness of all res­ above the sacrum (common), or if regions of the spine move as a 'block' instead of in a sequential wave-like man­ piratory muscles available in the supine position, includ­ ner, this can be noted as the current representation of a ing the following tha t are either involved in respiration dysfunctional pattern, as it involves thoracic spinal move­ or which - if shortened - could interfere with normal res­ ment. Areas moving en bloc are commonly those areas that pira tory function: pectoralis major, latissimus dorsi, ster­ were observed not to flex fully in the seated assessmen t. nomastoid, psoas (since this merges with the diaphragm). 4. The practitioner stands at waist level while facing the head and places the hands fully extended on each side of Figure 5. 1 0 I nferior thoracic apert u re and the dia p h rag m . Reproduced with permission from Gray's Anatomy for Students (2005). Lateral arcuate ..-;l\"'-�jiW Esophageal opening ligament --=;.:I-� ---,RI\\<c'�;> Costal margin 1r-�.-.I{!�qj Median arcuate ligament .�ji�iO-\"; Medial arcuate ligament Right crus ---.t�1i 1-1�-'-r:;=!\" Left crus -t-- Quadratus lumborum --'1\"'-1 Psoas major

94 CLINICAL APPLICATION OF NEUROMU SCULAR TECHNIQ UES: THE U P P ER BODY 2. The practitioner can now palpate and evaluate for trigger Box 5.2 Trigger point chains (Hong 1 994) point activity in muscles available in the prone pOSition tha t are associated with respiration or which - if short­ When key trigger points were deactivated, Hong noted that ened - could interfere with normal respiratory function. trigger points in d istant areas, which had previously tested as active, became inactive. The findings from these assessments point toward what is necessary in therapeutic or rehabilita tion terms as part of Deactivated trigger Inactivated associated triggers breathing retraining (Chaitow et al 2002). Sternocleidomastoid Upper tra pezius Tem pora lis, masseter, digastric TRIGGER POINT CHAINS (Mense 1 993, Patterson 1 976, Simons et al 1 999, Trave l l Et Si mons 1 992) Sca len ii Tem pora lis, masseter, splenius, semispinalis, levator scapulae, As compensatory postural patterns emerge, such as Janda's Splenius ca pitis rhomboid minor crossed syndromes which involve distinctive and (usually) S u p ra s p i n a t u s easily identifiable rearrangements of fascia, muscle and Infra s p i n a t u s Deltoid, extensor carpi radia lis, joints, it is inevitable that local, discrete changes should also Pectoralis minor extensor digitorum com munis evolve within these distressed tissues. Such changes include areas that, because of the particular stresses imposed on Latissimus dorsi Tem pora lis, sem ispinalis them, have become irrita ted and sensitized. Serratus posterior su perior Deltoid, extensor carpi radialis If particular local conditions apply (see Chapter 6), these irritable spots may eventually become hyperreactive, even Deep paraspinal Biceps brachii reflexogenically active, and mature into major sources of muscles (L5-Sl ) pain and dysfunc tion. This form of dysfunctional adapta­ Flexor carpi rad ial is, flexor carpi tion can occur segmentally (often involving several adjacent Quadratus lumborum u l na ris, first dorsal interosseous spinal segments) or in soft tissues anywhere in the body (as piriformis myofascial trigger points). The activation and perpetuation Piriformis Triceps, flexor carpi ulnaris of myofascial trigger points now becomes a focal point of H a mstri ngs even more adaptational changes. Triceps, latissimus dorsi, extensor digitorum communis, extensor carpi Clinical experience has shown tha t trigger point 'chains' ulnaris, flexor carpi ulnaris emerge over time, often contributing to predictable patterns of pain and dysfunction. Hong (1994), for example, has Gluteus maximus, medius, m i n imus; shown in his research that deactivation of particular trigger piriformis, hamstrings, tibialis, points (by means of injection) effectively inactivates remote peroneus longus, soleus, triggers (see Box 5.2). In the next chapter the trigger point g a stroc n e m i u s phenomenon will be examined in some detail. Gluteus maximus, medius, minimus; Hamstrings Peroneus longus, gastrocnemi us, soleus References Hamaoui A, Do M, Poupard L et al 2002 Does respiration perturb body balance more in chronic low back subjects that in healthy Chaitow L 1996 Muscle energy techniques. Churchill Livingstone, subjects? Clinical Biomechanics 1 7:548-550 Edi.nb urgh Hannon J 2006 Wartenberg's pend ulum: repose and the gripped Chai tow L 2004 Breathing pa ttern disorders, motor control and low patella (part 1 ) . Journal of Bodywork and Movement Therapies back pain. Journal of Osteopathic Medicine 7(1) :33-40 1 0 ( 1 ) : 35-50 Chaitow L, Bradley D, Gilbert C 2002 Multidisciplinary approaches Heinking K, Jones III J M, Kappler R 1997 Pelvis and sacrum. to breathing pa ttern disorders. Churchill Livingstone, Edinburgh In: Ward R (ed) Foundations for osteopathic medicine. American Osteopathic Association. Williams and Wilkins, Cholewicki ), Silfies S 2005 Clinical biomechanics of the lumbar Baltimore spine. In: Boyling J, Jul l G (eds) Grieve's modern manual ther­ Hong C-Z 1994 Considerations and recommendations rega rding apy: the vertebral column, 3rd edn . Churchill Livingstone, myofascial trigger point injection. Journal of Musculoskeletal New York Pain 2(1):29-59 Fowler E, Ho T, Nwigwe A, Dorey F 2001 The effect of quadriceps femoris muscle strengthening exercises on spastici ty in children Janda V 1982 Introduction to functional pathology of the motor sys­ with cerebral palsy. Physical Therapy 81 (6):l215-1223 tem. Proceedings of the VII Commonwea l th and Internationa l Gray's anatomy for students 2005 Churchill Livingstone, Con ference on Sport. Physiotherapy in Sport 3:39 Edinburgh Grieve G 1986 Modern manual therapy. Churchill Livingstone, Janda V 1983 Muscle function testing. Butterworths, London London

5 Patterns of dysfunction 9 5 Janda V 1986 Extracranial causes of facial pain. Journal of Prosthetic Mense S 1993 Peripheral mechanisms of muscle nociception and Dentistry 56(4):484-487 local muscle pain. Journal o f Musculoskeletal Pain 1 ( 1 ) : 1 33-170 Janda V 1988 Muscles and cervicogenic pain syndromes. In: Grant Mense S, Simons D 2001 Muscle pain: lmderstanding its nature, R (ed) Physical thera py in the cervical and thoracic spine. diagnosis, and treatment. Lippincott Williams and Wilkins, Churchill Livingstone, New York Philadelphia Janda V 1996 Evaluation of muscular balance. In: Liebenson C (ed) Morris C, Chaitow L, Janda V 2006 Functional examination of low Rehabil itation of the spine. Williams and Wilkins, Baltimore back syndromes. In: Morris C (ed) Low back syndromes. McGraw-Hill, New York Janda V, Frank C, Liebenson C 2006 Evaluation of muscular imbal­ ance. In: Liebenson C (ed) Rehabilitation of the spine, 2nd edn. Palastanga N, Field D, Soames R 2002 Anatomy and human move­ Lippincott Williams and Wilkins, Baltimore ment, 4th edn. Butterworth-Heinemann, Oxford, p 478--479 Jull G, Janda V 1987 M uscles and motor control in low back pain: Patterson M 1976 Model mechanism for spinal segmental faci l ita­ assessment and management. In: Twomey L, G rieve G (eds) tion. Academy of Applied Osteopathy Yearbook, Colorado Physical therapy of the low back. Churchill Livingstone, Springs, CO Edinburgh, p 253-278 Simons D, Mense S 1998 Understanding and measurement of mus­ Komendantov G 1945 Proprioceptivnije reflexi glaza i golovy u cle tone as related to clinical muscle pain. Pain 75( 1 ) : 1-17 krolikov. Fiziologiceskij Zurnal 31 :62 Simons D, Travell L Simons L 1999 Myofascial pain and dys fLU1c­ Kuchera M, Goodridge J 1997 Lower extremity. In: Ward R (ed) FOLU1dations for osteopathic medicine. American Osteopathlc tion: the trigger point manual, vol l : upper half of body, 2nd Association. Williams and Wil k ins, Baltimore edn. Williams and Wilkins, Baltimore Travell J, Simons D 1992 Myofascial pain and dysfunction, vol 2 . Lakie M, Tsementzis S, Walsh E 1980 Anesthesia does not (and can­ Williams and Wilkins, Baltimore not) reduce muscle tone? Journal of Physiology 30l:32 Vasilyeva L, Lew it K 1996 Diagnosis of m uscular dysfunction b y inspection. I n : Liebenson C (ed) Rehabilita tion of the spine. Le Cavorzin P, Poudens S, Chagneau F et al 2001 A comprehensive Williams and Wilkins, Baltimore model o f spastic hypertonia derived from the pend u l um test of Vogt L, Banzer W 1997 Dynamic testing of the motor stereotype in the leg. Muscle and Nerve 24( 1 2 ) : 1 6 1 2-1621 prone hlp extension from the neutral position. Clinical Biomechanics 12(2):1 22-127 Lehman G, Lennon D, Tresidder B et al 2004 Muscle recruitment Wachter K, Kaeser H, G u hring H et a l 1996 Muscle damping meas­ patterns during the prone leg extension test. BMC ured w i th a modi fied pendulum test in patients with fibromyal­ Musculoskeletal Disorders 5:3 gia, lumbago, and cervical syndrome. Spine 21(18):21 37-2142 War tenberg R 1951 Pendulousness of the legs as a diagnostic test. Lewit K 1999 Manipulative therapy in rehabilitation of the locomo­ Neurology 1 : 1 8-24 tor system, 3rd edn. Bu tterworths, London Liebenson C 2006 Rehabilitation of the spine, 2nd edn. Lippincott Williams and Wilkins, Baltimore

97 Chapter 6 Trigger points CHAPTER CONTENTS Neuromuscular therapy and neuromuscular technique (both unfortunately abbreviated as NMT) have among their key Ischemia and muscle pain 101 aims the removal of sources of pain and dysfunction. Ischemia and trigger point evolution 1 02 Modern pain research has demonstrated that a feature of all chronic pain is the presence (often as a major part of etiology) Trigger point connection 102 of localized areas of soft tissue dysfunction that promote pain Microanalysis of trigger poi n t tissues 1 03 and distress in distant structures (Melzack & Wall 1988). Ischemia and fibromyalgia synd rome (FMS) 1 03 These are the loci known as trigger points, the focus of enor­ FMS and myofascial pai n 1 0 5 mous research effort and clinical treatment. This chapter has Facilitation - segmental a n d l ocal 105 as its primary objective the task of suranru rizing current Trigger points and organ dysfu nction 1 06 knowledge and thinking on this topic. How to recognize a facilitated spinal area 1 08 Local facilitation in muscles 1 08 A great deal of research into the trigger point phenome­ Lowering the n eu ra l threshold 1 09 non - much of it outlined in this chapter - has been con­ Varying viewpoints on trigger poi nts 1 09 ducted worldwide since the first edition of Travell & Awad's analysis of trigger poi nts 1 09 Simons' (1983a) Myofascial Pain and Dysfunction: The Trigger Nimmo's receptor-tonus techn iques 1 09 Point Manual, Volume 1: Upper Halfof the Body was released I m proved oxygenation and reduced trigger poi n t pain - a n by Williams and Wilkins. That book and its companion vol­ ume for the lower extremities, published in 1992, rapidly example 110 became the preeminent resource relative to myofascial trig­ Pa i n-spasm-pa in cycle 1 1 0 ger points and their treatment. Volume 1 was updated in a Fibrotic scar tissue hypothesis 1 1 0 second edition in 1999 (Simons et all to include considerable Muscle spindle hypothesis 1 1 0 revisions in content and platform. Radiculopathic model for muscular pain 1 11 Simons' current perspective: an i ntegrated hypothesis 1 1 1 In the second edition of volume 1 of the Trigger Point Central and attachment trigger points 1 1 2 Manual, Simons et al (1999) have built on more recent Primary, key and satellite trigger points 1 1 2 research to modify not only the concepts around the theo­ Active and latent trigger points 1 1 3 retical basis of trigger point formation but also the most use­ Essential and spill over target zones 1 1 4 ful treatment protocols. Changes in technique application, Trigger points and joi n t restriction 1 1 4 including emphasis on massage and trigger point pressure Trigger points associated with shoulder restriction 1 1 4 release methods, accompany discussion of injection tech­ Other trigger poi nt sites 1 1 4 niques, so that appropriate manual methods are now far Testi ng a n d measuring trigger poi nts 1 1 4 more clearly defined. Suggested new terminology assists in Basic skil l requirements 1 1 5 clarifying differences and relationships between central Needle electromyography 1 1 6 (CTrP) and attachment (ATrP) trigger points, key and satel­ Ultrasound 1 1 6 lite trigger points, active and latent trigger points, and con­ Surface electromyography 1 1 6 tractures, which often result in enthesitis. Many of these Algometer use for research and clinical train ing 1 1 7 definitions have been incorporated in this text to encourage Thermography and trigger points 11 7 the development of a common language among practition­ Clinical features of myofascial trigger points 1 1 8 ers regarding these mechanisms. Developing skills for TrP pa lpation 1 1 9 Which method i s more effective? 1 21

98 C LI N I CA L A P PL I CAT I O N OF N E U R O M U S C U LA R T EC H N I Q U ES: T H E U P P E R B O DY In their second edition, Simons et al (1999) present an • analyzed and in some instances refuted previous research explanation as to the way they believe myofascial trigger into the area of myofascial trigger points, some of which points form and why they form where they do. Combining they assert was poorly designed information from electrophysical and histopathological sources, their integrated trigger point hypothesis appears to • suggested future research direction and design. be based solidly on current understanding of physiology and function. Additionally, the authors have: Simons et al (1999) present evidence which suggests that what they term 'central' trigger points (those forming in the • validated their theories using research evidence belly of the muscle) develop almost directly in the center of • cited older research (some dating back over 100 years) as the muscle's fibers, where the motor endplate innervates it at the neuromuscular junction (Fig. 6.1). They postulate the referring to these same mechanisms (see Box 6.1 for a following. brief historical summary) Box 6.1 Historical research into chronic referred muscle pain (Baldry 1993, Cohen Et GibbOns 1998, Simons 1988, 2004, Straus 1991, Van Why 1994) • F Va l l eix 1 841 Treatise on neuralgia. Paris (never substa ntiated) and suggested that pa i n sensations Noted that when certa i n pa i nfu l points were pal pated they pro­ emanati n g from nod u l es cou ld be due to nerve pressure (now d uced shooting pai n to other reg ions (neurolgia). H e also reported d iscounted). that diet was a precipitating factor in the development of th e • Sir William Osler 1 909 Principles and practice of medicine. painfu l aching symptoms of the back and cervical reg ion. Appleton, New York Considered the pa infu l aspects of muscular rheumatism (myalgia) • Johan Mezger, mid-1 9th century (Haberl ing W 1 93 2 Johan Georg to i nvolve 'neuralgia of the sensory nerves of the muscles'. • W Tel l i n g 1 9 1 1 Nodular fibromyositis - an everyday affliction and Mezger of Amsterdam. Founder of modern scientific massage. its identity with so-called muscular rheumatism. Lancet 1 :154- 1 58 Medical Life) Ca l l ed the condition ' nodular fibromyositis. Dutch physicia n, developed massage techniques for treating 'nod­ • L Llewellyn, A Jones 1 9 1 5 Fibrositis. Rebman, New York u l es' and ta ut cord-l i ke bands associated with this condition. Broadened the use of the word 'fibrositis' to include other condi­ • T I n man 1 858 Remarks on myalgia or muscular pain. British tions including gout. Medical Jou rnal 407-408 :866-868 • A Schmidt 1 9 1 8 Muskelrheumatismus (Myalgiej. Marcus Et Was able to clearly state that radiating pa in in these conditions Webers Verlag, Bonn (myalgia) was i n d ependent of nerve rou tes. Book on muscular rheumatism, myalgia. • Uno Helleday 1 876 Nordiskt Medicinkst Arkiv 6 Et 8 (8) • F Albee 1 927 Myofascitis - a pathological explanation of any Swedish physician d escribed nod u l es as part of 'chron ic myitis'. apparently dissimilar conditions. American Jou rnal of Surg ery • H Strauss 1 898 Kl i n ische Wochenschrift 3 5 :89-91 3:523-533 German physician distinguished between palpable nodules and Ca l l ed the condition 'myofascitis. 'bands'. • F Gudzent 1 93 5 Testunt und heilbehondlung von rheumatismus • I Adler 1 900 Muscular rheumatism. Medical Record 57:529-535 und gicht mid specifischen allergen. Deutsche Medizinsche Identified cli nical phenomena characteristic of MTrPs as muscular Wochenschrift 61 :901 rheumatism. German physician noted that chron ic 'muscular rheumatism' may • A Cornelius 1 903 Narben und Nerven. Deutsche M i l i ta ra rztlische at times be allergic in orig i n and that removal of certai n foods Zeitschrift 32:657-673 from the diet resulted in clinical improvement. German physician who demonstrated the pain-i nfl uencing fea­ • M Lange 1 931 Die Muskelharten (Myogelosenj. J F Lehmann's tures of tender points and n od u l es, i nsisti ng that the rad iating Verlag, Munchen pathway was not determi ned by the course of nerves. H e also First trigger poi nt manual. showed that external i nfluences, i ncluding climatic, emotional or • C H u nter 1 933 Myalgia o f the abdominal wall. Canadian Medical physical exertion, could exacerbate the already hyperreactive Association Journal 28:1 57-1 61 neural structu res associated with these conditions. Cornelius Described referred pa i n (myalgia) resulting from tender points sit­ also d iscussed these pain phenomena as being d ue to reflex uated i n the abdominal musculature. • J Edeiken, C Wolferth 1 936 Persistent pain in the shoulder region mechanisms. following myocardial infarction. American Journal of Med i cal Science 191 : 20 1 -210 • A M u l ler 1 9 1 2 Untersuchungsbefund am rheumatische erkronten Showed that pressure applied to tender points i n scapula region muskel. Zeitschrift Kl i n ische Medizin 74:34-73 muscles cou ld reproduce shou lder pa in already bei ng experienced. German physician who n oted that to identify n od u l es and bands This work i nfl u enced Janet Travel l - see bel ow. req u i red refined palpation skills, aided, he suggested, by l ubricat­ ing the skin. • Sir Thomas Lewis 1 938 Suggestions relating to the study of somatic pain. B ritish Medical Jou rnal 1 :321 -325 • Sir William Gowers 1 904 Lumbago: its lessons and analogues. A major researcher into the phenomenon of pa i n in general, British Medical Jou rnal 1 : 1 1 7- 1 21 charted severa l patterns of pa in referral and suggested that Suggested that the word fibrositis be used, believing erroneously Kel lgren (see below). who assisted him in these studi es, conti nue that inflammation was a key feature of 'muscular rheumatism'. the research. Lecture, National Hospital of Nervous Diseases, London. • Ralph Stockman 1 904 Causes, pathology and treatment of chronic rheumatism. Edinburg h Med i ca l Jou rnal 1 5 : 1 07-1 1 6, 223-225 Offered support for Gowers' suggestion by reporting finding evidence of inflammation i n con nective tissue i n such cases box continues

6 Trigger points 99 Box 6.1 (continued) trial ingestion of allergenic foods or inhalation of house dust • J Kellgren 1938 Observations on referred pain arising from muscle. extract or particu lar hydrocarbons, with rel ief of symptoms often Clinical Science 3 :17 5 -190 being achieved by avoidance of a l l ergens. Randolph reports that Identified (in patients with 'fibrositis' and 'myalgio' ) many of the severa l of his patients who achieved rel ief by these means had features of our current understanding of the trigger point phe­ previously been d iagnosed as having 'psychosomotic rheumatism'. nomenon, incl ud ing consistent patterns of pain referra l - to dis­ • James Menne l l 1 9 5 2 The science and art of joint manipulation, tant muscles and other structures (teeth, bone, etc.) from pain vol 7. Churchi l l , London points ('spots') in muscle, ligament, tendon, joint and periosteal British physician described 'sensitive areas' which referred pain. tissue - which could be obliterated by use of novocaine Recommended treatment was a choice between manipu lation, i njections. heat, pressure and deep friction. He a l so em phasized the impor­ tance of diet, fluid intake, rest, the possible use of cold and pro­ • A Reichart 1938 Reflexschmerzen auf grund von myoglosen. caine injections as well as suggesting cupping, skin rol l ing, Deutsche Medizinische Wochenschrift 64 :823 -824 massage and stretching in norma lization of' fibrositic deposits'. Czech physician who identified and charted patterns of distri bu­ • Janet Travel l (and S Rinzler) 19 52 The myofascial genesis of pain. tion of reflex pain from tender points (nodu les) in particu lar Postgrad uate Medicine 11 :425-434 muscles. B u i lding on previous research and fol l owing her own detailed studies of the tissues involved, coined the word 'myofascial', • M Gutstein 1 938 Diagnosis and treatment of muscular rheuma­ adding it to Steind ler's term to produce 'myofascial trigger points' tism. British Journal of Physical Medicine 1 :302-321 and fina l ly ' myofascial pain syndrome'. Between 1 942 and 1 993, Refugee Polish physician working in Britain who identified that in Janet Travel l authored four books and more than 1 5 papers on treating muscular rheumatism, manual pressure applied to tender TrPs; however, it was this paper that introduced referra l patterns (later ca l led 'trigger') points produced both local and referred for 32 m u scles. Only one paper prior to her 1 983 book had a symptoms and that these referra l patterns were consistent in minor mention of a loca l twitch response. everyone, if the original point was in the same location. He deac­ • I Neufeld 1 9 5 2 Pathogenetic concepts of 'fibrositis' - fibropathic tivated these by means of injection. His other papers publ ished syndromes. Archives of Physical Medicine 3 3 :363 -369 between 1 938 and 1 9 51 identified the cond ition with 11 different Suggested that the pain of 'fibrosistis-fibropathic syndromes' was names, including common rheu matism, idiopathic mya lgia, rheu­ due to the brain misinterpreting sensations. matic mya lgia, myalgia, muscu lar sciatica, fibrositis, a m uscle dis­ • F Speer 1954 The allergic-tension-fatigue syndrome. Pediatric ease and non-articu lar rheumatism (see below as Gutstein-Good Clinics of North America 1 :1029 -1 037 and as Good). Called the cond ition the 'allergic-tension-fatigue syndrome' and added to the pain, fatigue and general sym ptoms previously rec­ • A Steindler 1 940 The interpretation of sciatic radiation and the ognized (see Randolph above) the observation that edema was a syndrome of low back pain. Journal of Bone and Joint Su rgery feature, especially involving the eyes. 22:28-34 • R Gutstein 1 9 5 5 Review of myodysneuria (fibrositis). American American orthopedic surgeon who demonstrated that novoca ine Practitioner 6 :570-577 injections into tender points located in the low back and gluteal Called the cond ition' myodysneurio'. regions cou l d relieve sciatic pain. H e ca lled these points 'trigger • R Nimmo 1 9 57 Receptors, effectors and tonus: a new approach. points'. Janet Travell (see below) was infl uenced by his work and Journal of the National Chiropractic Association 27( 1 1 ) :21 popularized the term 'trigger points'. After many years of research, which paralleled chronologically that of Travell, he described his concept of 'receptor-tonus technique', • M Gutstein-Good 1 940 (sa me person as M Gutstein above) involving virtua l ly the same mechanisms as those eventually Idiopathic myalgia simulating visceral and other diseases. Lancet described by Travell Et Simons (1 983a) but with a more manual 2:3 26 -3 28 emphasis. 'I have found that a proper degree of pressure, sequential ly Ca lled the cond ition 'idiopathic myalgio'. applied, causes the nervous system to release hypertonic muscle: • M Kel ly 1 962 Local injections for rheumatism. Medical Journal of • M Good 1 941 (same person as M Gutstein and M Gutstein-Good Austra lia 1 :45 -50 above) Rheumatic myalgias. The Practitioner 1 46 :1 67 -1 74 Austra l ian physician who carried on Kellgren's concepts from the Ca lled the cond ition 'rheumatic myalgio'. early 1 940s, diagnosing and treating pain (rheumatism) by means of identification of pain points and deactivating these using • James Cyriax 1 948 Fibrositis. British Medical Journal 2:251 -255 injections. Believed that chronic muscle pain derived from nerve im pinge­ • M Yunus et al 1981 Primary fibromyalgia (fibrositis) clinical study ment due to d isc degeneration. 'It [pressure on dura mater] has of 50 patients with matched controls. Seminars in Arthritis and misled clinicians for decades and has given rise to endless m isd i­ Rheumatism 1 1 :1 51 -1 71 agnosis; for these areas of \"fibrositis\", \"trigger points\", or \"mya l­ First popu larized the word 'fibromyalgio'. gic spots\", have been regarded as the primary lesion - not the • Janet Travel l , David Simons 1 983 Myofascial pain and dysfunc­ resu lt of pressure on the dura mater' (Cyriax J 1 962 Textbook of tion: the trigger point manual vol 7. Wi l l iams and Wilkins, orthopaedic medicine, vol 1, 4th edn. Cassell, London). B a l t i more The definitive work (with vol u me 2, 1 99 2) on the subject of • P Ell man, D Shaw 1 9 50 The chronic 'rheumatic' and his pains . myofascial pain syndrome (MPS). • K Lewit, D Simons 1 984 Myofascial pain: relief by post-isometric Psychosomatic aspects of chronic non-articular rheumatism. relaxation. Archives of Physical Medicine and Rehab i l i tation 6 5 :4 52-456 Anna ls of Rheumatic Disease 9 :341 -3 57 Czech neurologist Karel Lewit described his simple manual treat­ Suggested that because there were few physical manifestations ment of MTrPs, and later emphasized joint dysfunction in MTrPs to support the pain cla imed by patients with chronic muscle pain, their cond ition was essentially psychosomatic (psychogenic box continues rheumatism): 'the patient aches in his l i mbs because he aches in his mind'. • Theron Randolph 1 9 51 Allergic myalgia. Journal of Mich igan State Med ical Society 50:487 This lead ing American clinical ecologist described the cond ition as allergic myalgia and demonstrated that widespread and severe muscle pain (particularly of the neck region) could be reproduced 'at will under experimental circu mstances' following

1 00 C L I N I C A L A P P L I C AT I O N O F N E U R O M U S C U L A R T EC H N I QU ES: T H E U P P E R B O DY [ with suggestions as to joi n t mobilization, and later developed Showed that many 'tender points' in fibromyalgia are i n va luable concepts of cha ins of MTrPs. rea l ity latent trigger poi nts. He believes t h a t MPS and FMS • David Si mons 1 986 Fibrositis/fibromyalgia: a form of myofascial are d istinctive syndromes but are 'closely related'. States that trigger points? American Journal of Med icine 81 (Su ppl 3A):93 -98 many people with MPS progress on to develop fibromyalgia. American physician who collaborated with Travel l in a joint study • C-Z Hong 1 994 Electrophysical characteristics af localized twitch of MPS and who a lso conducted his own studies i nto the con nec­ tion between myofascial pain syndrome a n d fibromyalgia syn­ responses in responsive taut bands of rabbit skeletal muscle. drome, finding a good deal of overlap. • M Margoles 1 989 The concept of primary fibromyalgia. Pain Journal of Musculoskeletal Pain 2(2) :1 7-43 3 6 :391 -39 2 This physiatrist pioneered studi es focusing on identifying taut States t h a t most patients w i t h fibromyolgio demonstrate n umer­ bands of MTrPs. ous active myofascial trigger points. • D Simons, J Travel !, L Simons 1999 Myofascial pain and dysfunc­ • R Bennett 1 990 Myofoscial pain syndromes and the fibromyalgia tian: the trigger point manual, vol 1: upper half of body, 2nd edn. syndrome. In: Fricton R, Awad E (eds) Advances in pain research Wi l l iams & Wilki ns, Baltimore This second edition, with emphasis on sig nificant research con­ and therapy. Raven Press, New York ducted in the 1 5 years since the first edition, altered the founda­ tional platform of trigger poi nt theories and trea tment. Figure 6.1 I ntegrated hypothesis of e n d pla te dysfunction associated with trigger point formation. SR, sarcop l asm ic reticu l u m . Adapted from Simons et a l (1999). Motor nerve terminal Excess acetylcholine release -\"\"-' Depolarization =f'=I::=: +=1=;=d==-==::=��';��5d���:;�; Calcium release �'$ Sarcomere contracture Compression of vessels • Dysfunctional endplate activity occurs (commonly asso­ • As the endplate keeps producing ACh flow, the actin/ ciated with a strain), which causes acetylcholine (ACh) to myosin filaments slide to a fully shortened position (a be excessively released at the synapse, often associated weakened state) in the immediate area around the motor with excess calcium. endplate (at the center of the fiber). • The presence of high calcium levels apparently keeps the • As the central sarcomeres shorten, they begin to bunch calcium-charged gates open and the ACh continues to be and a contracture 'knot' forms. released, resulting in localized ischemia. • This knot is the 'nodule' that is a palpable characteristic • The consequent ischemia involves an oxygen/nutrient of a trigger point (Fig. 6.2). deficit that, in turn, leads to a local energy crisis and inadequate adenosine triphosphate (ATP) production in • As this process occurs, the remaining sarcomeres of that the immediate area. fiber (those not btffiching) are stretched, thereby creating the usually palpable taut band that is also a common trig­ • Without available ATP the local tissue is unable to remove ger point characteristic. (active transport) the calcium ions that are 'keeping the gates open', thereby allowing continued release of Ach. • Attachment trigger points may develop at the attachment sites of these shortened tissues (periosteal, myotendinous) • Removing the superfluous calcium requires more energy where muscular tension provokes inflammation, fibrosis than sustaining a contracture, so the contracture remains. and, eventually, deposition of calcium. • The resulting muscle fiber contracture (involuntary, This model is explored in greater depth later in this chapter, without motor potentials) is distinctly different from a since it represents the most widely held understanding as to contraction (voluntary, with motor potentials) and spasm the etiology of myofascial trigger pOints. Other models exist (involuntary, with motor potentials). which attempt to explain the trigger point phenomenon, including the facilitation concept (below) and the ideas • The contracture is apparently sustained by the chemistry and methods developed by Raymond Nimmo DC (1981) at the innervation site, not by action potentials from the spinal cord.

6 Trigger poin ts 1 0 1 Trigger point complex are released to act on vessels and nerves locally. These include catecholamines, serotonin, histamine, bradykinin Taut band Nodule and prostaglandins. Among their effec ts, these substances cause vasodilation and vascular permeabili ty, often resu lt­ A ing in local edema. As edema increases, arterial and venous vessels are compressed, resulting in a vicious cycle that B Contraction further reduces blood supply and sensitizes nociceptors. knot Research also shows that when pain receptors are stressed (mechanically or chemically) and are simultaneously exposed Normal to elevated levels of adrenaline, their discharge rate increases, fibers i .e. a greater volume of pain messages is sent to the brain (Kieschke et al 1988). Figure 6.2 ARB : Tension produced by central trigger point (CTrP) \\tV-hen the blood supply to a muscle is fully inhibited, can result in localized inflammatory response (attachment trigger pain is not usually noted until that muscle is asked to con­ tract, at which time pain is likely to be noted within 60 sec­ point, ATrP). Adapted from Simons et al (1 999). onds (Mense et aI2001). This is the phenomenon that occurs in intermittent claudication. The precise mechanisms are (discussed below) . Before examining these, it will be useful open to debate but are thought to involve one or more of a to investigate a key element of myofascial trigger point number of processes, including potassium ion build-up, the development and dysfunction - ischemia. lack of oxidation of metabolic products and the release of algesic substances. Previous concepts of lactate accumula­ ISCHEMIA AND MUSCLE PAIN tion have now been discarded as a maj or factor in ischemic muscle pain since it is considered to be an ineffec tive activa­ Ischemia can be simply described as a state in which the tor of muscle nociceptors, although it may have a combined current blood supply is inadequate for the current physio­ action with other substances (Mense et aI2001). Further, lac­ logical needs of tissue. The causes of ischemia can be patho­ tate (or lactic acid) accumulation following rigorous exer­ logic, as in a narrowed artery or thrombus, or anatomic, as cise does not appear to be the cause of delayed onset muscle in particular hypovascular areas of the body, such as the soreness (12-24 hours) since concentrations rapidly region of the supraspinatus tendon 'between the anastomo­ decrease within 1 hour following cessation of exercise sis of the vascular supply from the humeral tuberosity and (Khalsa 2004). the longitudinally directed vessels arriving from the muscle's belly' (Tullos & Bennet 1984), or as a result of a sequence of Pain receptors are sensitized when under ischemic condi­ events such as occurs in trigger point development outlined tions (i t is thought) due to the release of algesic substances above. Compression of blood vessels or blockage of blood such as bradykinin, a chemical mediator of inflammation. flow by any means can result in ischemia and excitation of This has been confirmed by the use of drugs that inhibit nociceptors. bradykinin release, allowing an active ischemic muscle to remain relatively painless for longer periods of activity The development of ischemia in muscles can be immedi­ (Oigiesi et aI1975). When ischemia ceases, pain receptor acti­ ate, such as results when trauma occurs, or can be slow and vation persists for a time and, conceivably, indeed probably, insidious, such as that associated with postural adaptation. contributes to sensitization (facilitation) of such structures, a Pain receptors are stimulated (and become sensitized) by phenomenon noted in the evolution of myofascial trigger prolonged intense muscular contraction when biological points (discussed further below). substances, known as vasoneuroactive substances (VNS), Although ischemic muscles may remain painless LUltil asked to contract, trigger points in muscle may refer pain even when the muscle is not being actively used. The term 'essential pain zone' describes a referral pattern that is pres­ ent in almost every person when a particular trigger point is active. Some trigger points may also produce a 'spillover pain zone' beyond the essential zone, or in place of it, where the referral pattern is usually less intense (Simons et aI1999). These target zones should be examined, and ideally pal­ pated, for changes in tissue 'density', temperature, hydrosis and other characteristics associated w ith satellite trigger point formation (as discussed later in this chapter). Trigger point activity itself may also induce relative ischemia in the 'target' tissues (Baldry 1993, Simons et aI1999). The mechanisms by which this occurs remain hypothetical

1 02 C LI N I CA L APPLICAT I O N OF N E U RO M U SCULAR T E C H NIQU ES: T H E U P PER B O DY but may involve a neurologically mediated increase in tone in sidelying sleeping posture, may lead to relative ischemia in the trigger point's reference zone (target tissues). According under the acromion process (Brewer 1979). These are pre­ to Simons et al (1999) these target zones are usually periph­ cisely the sites most associated with rotator cuff tendinitis, eral to the trigger point, sometimes central to the trigger calcification and spontaneous rupture (Cailliet 1991), as point and, more rarely (27%), the trigger point is located well as trigger point activi ty. within the target zone of referral. This is more than informa­ tional as it translates to a significant clinical application: if Additionally, a number of shoulder and neck muscles, the practitioner is treating only the area of pain and the including levator scapulae, anterior and middle scalenes, tri­ cause is myofascial trigger points, he is 'in the wrong spot' ceps brachii and trapezius, target the supraspinatus area as nearly 75% of the time! their referred zone and can produce not only pain but also autonomic and motor effects, including spasm, vasoconstric­ Any appropriate manual treatment, movement or exer­ tion, weakness, loss of coordination and loss of work toler­ cise program that encourages normal circulatory function is ance in the target tissues (Simons et aI1999). Due to weakness likely to modulate these negative effects and reduce trigger and loss of coordination, the person may adapt by improp­ point activity. It is important to note, however, that when erly using these and other muscles with resultant damage to tissues containing (particularly active) trigger points are the tissues (see patterns of dysfunction, Chapter 5). exercised prior to the deactivation of the trigger points, the referred pain is often provoked or increased . Therefore, a TRIGGER POINT CONNECTION general protocol suggests that manual palpation, examina­ tion for and treatment of trigger points, would precede the Mense (1993) describes the hypothesized evolution of a trig­ start of exercise therapy. After treatment of trigger points ger point, clearly similar to the Simons et al (1999) model. and elongation of the taut bands housing them, a condition­ ing program can be implemented to help prevent reactiva­ A muscle lesion leads to the rupture of the sarcoplasmic tion. A degree of normal function may return when the soft reticulum and releases calciumfrom the in tracellular stores. tissue's Circulatory environment is improved and the stress­ The increased calcium concentration causes sliding of the producing elements, whether of biomechanicaL biochemi­ myosin and actin filaments; the result is a local contracture cal and/ or psychosocial origin, are reduced or removed. (myofilamen t activation without electrical activity) that has high oxygen consumption and causes hypoxia. An addi­ Increased lymphatic flow, which is enhanced by light tionalfactor may be the traumatic release ofvasoneuroactive gliding strokes and other forms of tugging on the skin sur­ substances (for example, bradykinin), which produce local face, such as that created by manual lymph drainage tech­ edema that in turn compresses venules and enhances the niques (Chikly 2001 , Wittlinger & Wittlinger 1982), will ischemia and hypoxia. Because of the hypoxia-induced drop assist in draining the waste materials that accumulate in ATP concentrations, thefunction of the calcium pump in within the ischemic tissues, while altering the local cellular the muscle cell is impaired, and the sarcoplasmic calcium chemistry and reducing neuroexcitation. Many massage concentration remains elevated. This perpetuates the con­ techniques drain lymphatic wastes; however, some are tracture. designed to dynamically induce lymph movement and drainage (Chikly 1996, 2001, Wittlinger & Wittlinger 1982). The presence of oxygen deficit at the heart of the trigger Use of these specialized techniques, especially in a system­ point has been confirmed, according to Mense: atic protocol that addresses opening the primary pathways of lymph flow in a particular order, may greatly enhance the Measurements of the tissue p02 with microprobes show that conditions of the in terstitial fluids surrounding the cells. oxygen tension . . . is extremely low. Thus, the pain and Such movement may also i ncrease the flow of nutrients to tenderness of a trigger point could be due to ischemia­ the area, thus improving the cells' physiological status. induced release of bradykinin and other vasoneuroactive substances which activate and/or sensitize nociceptors. ISCHEMIA AND TRIGGER POINT EVOLUTION (Bruckle et a1 1990) Hypoxia (apoxia) involves tissues being deprived of ade­ The original 'lesion' could have been the result of any of the quate oxygen. This can occur in a number of ways, such as multiple etiological and maintaining factors (overuse, mis­ in ischemic tissues where circulation is impaired, possibly use, abuse, disuse) outlined in the overview of stress and due to a sustained hypertonic state resulting from overuse the musculoskeletal system in Chapter 4. It could be the or overstrain. The anatomy of a particular region may also result of a gross trauma, such as a blow, sudden elongation predispose it to potential ischemia, as described above in (as in whiplash) or laceration, occurring recen tly or even relation to the supraspinatus tendon. Additional sites of rel­ years before. It could also be the result of sustained emo­ ative hypovascularity include the insertion of the infra­ tional distress, with its influence on somatic structures, or of spinatus tendon and the intercapsular aspect of the biceps the effects of hormonal imbalance, specific nu tritional defi­ tendon. Prolonged compression crowding, such as is noted ciencies, aJlergic (or sensitivity) reactions or increased levels of toxic material in the tissues (see Chapter 4).

6 Trigger points 1 03 Simons describes the trigger point evolu tion as follows. EMG Visualize a spindle like a strand ofyarn in a knitted sweater . . . EMG twitch potential a metabolic crisis takes place which increases the tempera­ ture locally in the trigger point, shortens a minute part of A the muscle (sarcomere) - like a snag in a sweater - and reduces the supply of oxygen and nutrients into the trigger Tera�ki plate point. During this disturbed episode an influx of calcium occurs and the muscle spindle does not have enough energy B Muscle tissue to pump the calcium outside the cell where it belongs. Thus a vicious cycle is maintained; the muscle spindle can't Figure 6.3 ARB : An in-vivo microanalytical technique for measuring seem to loosen up and the affected m uscle can't relax. ( Wolfe the local biochemical milieu of human skeletal muscle. TP1, trigger et (1 1992) point 1 . Reproduced with permission from Shah et al (2005). MICROANALYSIS OF TRIGGER POINT TISSUES In a personal communication (2004), the lead researcher reported that pH levels returned to normal almost instantly Shah et al (2003, 2005) have developed a microanalytical when the taut band was released, i.e. when the biopsy nee­ technique that enables continuous sampling of extremely dle touched it, as did levels of oxygen. small quantities of substances directly from soft tissue. Three subjects were selected from each of three groups (total nine Commenting on this research, Simons (2006) stated: subjects): 'Remarkably, and unexpectedly, the clinical distinction betvveen active and latent MTrPs was sharply distinguished • Normal (no neck pain, no myofascial trigger points) by the concentration of these stimulants of nociception.' (See • Latent (no neck pain, myofascial trigger point present) also notes on needle electromyography later in this chapter.) • Active (neckpain, active myofascial trigger point present). ISCHEMIA AND FIBROMYALGIA A pressure algometer was used to record the pain threshold, SYNDROME (FMS) following which a microdialysis needle was inserted in a standardized location in the upper trapezius muscle on It has been suggested that the origin of the pain noted in each of the six people whose trigger points (three active, fibromyalgia may also derive in large part from muscular three latent) had been identified. Using ultrasound imaging ischemia (Heruiksson 1999). the hollow needle was moved, in very small stages, toward the heart of a trigger point (its taut band) until it touched the The rationale for this observation can be summarized as band. At each small stage of the needle's penetration of the follows: tissues, samples were taken of the tissue fluids. • The pathophysiology of the chronic muscular pain and The same region of upper trapezius was penetrated by tenderness of FMS is not fully understood, but seems to the needle and samples taken, in the three people without trigger points, to compare the nature of the fluids extracted. In this way multiple samples, from the three groups, were obtained and could be compared. Analytes removed and tested showed that concentra­ tions of protons (H+), bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor, serotonin and norepinephrine were significantly higher in the active group than either of the other two groups (p < 0.01). Additionally, pH was significantly lower in the active group than the other tvvo groups (p < 0.03). To summarize the most important findings: • People with active trigger points had a very much lower pain threshold than the other individuals studied. • The tissues surrounding active trigger points had much higher levels of substances such as bradykinin, norepi­ nephrine and substance P than those with latent, or no, trigger points. • The level of acidity (pH) of the tissues in the region of the active trigger points was very much greater (i.e. there was lower pH) than the others tested.

1 04 C L I N I CA L A P P L I CATI O N OF N E U R O M U S C U LA R T EC H N IQ U ES: T H E U PP E R B O DY AB CD Figure 6.4 Doppler evaluation of intersegmental muscle ( I S M ) during static contraction in (A) healthy control subject and (B) FM patient, showing typical no or small vessel perfusion. I n (el. after the administration of ultrasound contrast media, the muscular tissue vascularity is clearly seen in the control subject. Differently in (D) the I SM of an FM patient shows no detectable flow during contraction. Note, however, that normal muscular vascularity is seen in the non-contracting deltoideus muscle in the upper right-hand corner. Reproduced with permission from Elvin et al (2006). involve complex interactions between peripheral and cen­ • In a study of this phenomenon (Elvin et al 2006) it was tral nervous system mechanisms, with evidence of abnor­ found that contrast-enhanced ultrasound was useful to mal processing of somatosensory input (Kosek & Hansson examine real-time muscle vascularity during and follow­ 1997). ing standardized, low-intensity exercise in fibromyalgia • Morphological abnormalities have long indicated that patients and healthy controls (Fig. 6.4). ischemia is a feature of these muscles (Bennett 1989). • Many FMS patients report a sensation of muscle 'feeling • FM patients had a reduced increase in muscular vascu­ swollen' during exercise. larity following dynamic exercise and during, but not fol­ • The circulatory dysfunction evident in muscles of FMS in lowing, static exercise compared to controls. relation to exercise (e.g. reduced muscle perfusion) appears to be accentuated by the relative deconditioned • The results support the suggestion that muscle ischemia status of people with FMS (McCain et aI1988). contributes to pain in fibromyalgia, possibly by main­ taining central sensitization/disinhibition.

6 Trigger points 1 05 Box 6.2 Fibromyalgia and myofascial pain Among the research into the connection between myofascial trigger 3. Researchers at Oregon Health Sciences U n iversity studied the point activity and fibromyalgia are the fol lowing: history of patients with FMS and fou nd that over 80% reported that prior to the onset of their genera l ized symptoms they 1. Yu nus ( 1 993) suggests that 'Fibromyalgia and myofascial pai n suffered from reg i onal pa i n problems (which almost always syndrome (MPS) [trigger point-derived pain] share several com­ involved trigger poi nts). Physical tra u ma was cited as the major mon features [and] it is possible that MPS represents an incom­ cause of their pre-FMS regi ona l pain. Only 1 8% had FMS plete, reg ional or early form of fibromyalgia syndrome since many which started without pri or reg iona l pain (Burckhardt fibromya lgia patients give a clear history of l ocalized pain before 1 995). developing generalised pain: 4. Research at UCLA has shown that injecting active trigger 2. Granges & Littlejohn (1 993) i n Austra l i a have researched the poin ts with the pa in-killing agent xyl ocaine produced marked overlap between trigger points and the tender poi nts in benefits in FMS patients in terms of pain rel ief and reduction of fibromyalgia and come to several conclusions, including: stiffness but that this is not rea lly sig nifica ntly a pparent for a t least a week after t h e injections. FMS patients reported more 'Tender points i n FMS represent a diffusely diminished pain thresh­ local soreness foll owing the injections than patients with only myofascial pain but improved after this settled down. Th is rein­ old ta pressure while trigger points are the expression of a local forces the opi nion of many practitioners that myofascial trigger musculoskeletal abnormality' points contribute a large degree of the pai n being experienced in FMS (Hong 1 996). 'It is likely that trigger points in diffuse chronic pain states such as 5. Travell & Simons (1992) are clearly of this opi n i on, stating 'Most FMS contribute only in a limited and localized way to decreasing of these [fibromya lgia] patients would be l ikely to have specific '\" myofascial pain syndromes that would respond to myofascial therapy: the pain threshold to pressure in these patients: 'Taken individually the trigger points are an important clinical finding in some patients with FMS with nearly 700;0 of the FMS patients tested having at least one active trigger point: 'Of those FMS patients with active trigger points, around 60% reported that pressure on the trigger 'reproduced a localized and familiar {FMS] pain: FMS AND MYOFASCIAL PAIN the cause of facilitation may be the result of organ dysfunc­ tion as explained below (Ward 1997). Having noted a clear connection between ischemia and myofascial pain, as well as a well-supported proposed link It has long been hypothesized in osteopathic medicine as betvveen ischemia and fibromyalgia, it would be useful to well as chiropractic care that organ dysfunction will result refer to Box 6.2 which looks at some of the suggested in sensitization and, ultimately, facilitation of the paraspinal relationships betvveen fibromyalgia and myofascial pain structures at the level of the nerve supply to that organ. The syndromes. term viscerosomatic reflex is well established to describe the consequences of this situation. If, for example, there FACILITATION - SEGMENTAL AND LOCAL is any form of cardiac disease, there will be a 'feedback' toward the spine of impulses along the same nerves that (Korr 1976, Patterson 1976) supply the heart and the muscles alongside the spine in the upper thoracic level (T2, T3, T4 as a rule) served by the same Neural sensitization can occur by means of a process known neural segments will become hypertonic. If the cardiac as facilitation. There are two forms of facilitation: segmental problem continues, the area will become facilitated, with (spinal) and local. If we are to make sense of soft tissue dys­ the nerves of the area, including those passing to the heart, function, we should have an understanding of facilitation. becoming sensitized and hyperirritable. Electromyographic readings of the muscles alongside the spine at this upper Facilitation occurs when a pool of neurons (premotor thoracic level would show this region to be more active than neurons, motoneurons or, in spinal regions, preganglionic the tissues above and below it. The muscles alongside the sympathetic neurons) is in a state of partial or subthreshold spine, at the facilitated level, would be hypertonic and excitation. In this state, a lesser degree of afferent stimula­ almost certainly painful to pressure. The skin overlying this tion is required to trigger the discharge of impulses. facilitated segmental area will alter in tone and function Facilitation may be due to sustained increase in afferent (with increased levels of hydrosis as a rule) and will display input, aberrant patterns of afferent input or changes within a reduced threshold to electrical stimuli. the affected neurons themselves or their chemical environment. Once established, facilitation (sensitization) can be sustained Research into the ability of osteopathic diagnostic meth­ without the involvement of central nervous system activity. ods to accurately identify such dysfunction has been carried It is the example of neurons maintained in a hyperirritable out and evaluated (Kelso et aI1980). Between 1969 and 1972 state, due to an altered biochemical status in their local envi­ over 6000 patients admitted to Chicago Osteopathic Hospital ronment, that appears to come closest to the situation occur­ were part of a clinical investigation. Visual and palpatory ring in trigger point behavior. On a spinal segmental level observations made by attending osteopathic physicians were recorded and analyzed in relation to the health problems

1 0 6 C L I N ICAL A P P L I CAT I O N O F N E U R O M USCU LA R T EC H N I Q U ES : T H E U P P E R B O DY L of the patients. The findings showed a clear link between stasis and edema, structural bodywork to reduce postural the spinal area, diagnosed by the examining practitioner as stress and relaxation techniques of biofeedback, hypnother­ being involved, and the corresponding diseased organs of apy or psychotherapy to reduce the number of signals from the patient. The conclusion was: 'The somatic findings in higher centers of the central nervous system. over 6,000 cases of hospital patients support the osteopathic theory of viscero-somatic (internal organs and the body) In assessing and treating somatic dysfunction, the phe­ relationships.' nomenon of segmental facilitation should always be borne in mind, since the causes and treatment of these facilitated seg­ In a separate study doctors at Riverside Osteopathic ments may lie outside the scope of practice of many practi­ Hospital in Trenton, Michigan, investigated the existence of a tioners and can easily be overlooked. In many instances, viscerosomatic reflex that could be easily detected and which appropriate manipulative treatment can help to 'destress' correlated with the presence of atherosclerotic coronary facilitated areas. However, when a somatic dysfunction con­ artery disease. Eighty-eight consecutive patients, each sug­ sistently returns after appropriate therapy has been given, the gesting coronary disease, underwent cardiac catheterization. possibility of organ disease or dysfunction is a valid consider­ Within 1 week of this, each patient in tum was given stan­ ation and should be ruled out or confirmed by a physician. dard osteopathic musculoskeletal evaluation (pain, range of movement, soft tissue texture, etc.) by an examiner unaware TRIGGER POINTS AND ORGAN DYSFUNCTION of the results of the cardiac catheter probe. Conditions that lie outside obvious musculoskeletal dys­ The results showed a correlation between coronary ath­ function may at times have trigger points as a primary fea­ erosclerosis and abnormalities of range of motion and soft ture. Selected examples include the following. tissue texture in the 4th and 5th thoracic and the 3rd cervi­ cal intervertebral segments. Chro n i c prostatitis Once facilitation of the neural structures of an area has Chronic prostatitis involving non-bacterial urinary difficul­ occurred, all associated target structures (connective tissue, ties, accompanied by chronic pelvic pain (involving the per­ muscle, bone, blood vessels, skin, sweat glands and internal ineum, testicles and penis), has been shown in a study at organs) can be adversely affected. Any additional stress of Stanford University Medical School to be capable of being any sort that impacts the individual, whether emotional, treated effectively using trigger point deactivation together physical, chemical, climatic, mechanical - indeed, absolutely with relaxation therapy (Anderson et aI2005). anything that imposes adaptive demands on the person as a whole and not just this particular part of their body - leads The researchers pOint out that 95% of chronic cases of to a marked increase in neural activity in the facilitated seg­ prostatitis are unrelated to bacterial infection and that ments and not in the rest of the normal, 'unfacilitated' spinal myofascial trigger points, associated with abnormal muscu­ structures. Different types of problem are associated with lar tension in key muscles, are commonly responsible for facilitated segments at specific levels - for example, T9/ 10 the symptoms. (gallbladder), T12/L l (kidney) and L5 (urogenital). The I-month study involved 138 men, and the results Korr (1976) has called such an area a 'neurological lens' produced marked improvement in 72% of the cases, with since it concentrates neural activity to the facilitated area, so 69% showing significant pain reduction and 80% improve­ creating more activity and also a local increase in muscle ment in urinary symptoms. The study noted that: tone at that level of the spine. Similar segmental (spinal) facilitation occurs in response to any organ problem, affect­ TrPs in the anterior levator ani muscle often refer pain to the ing only the part of the spine from which the nerves supply­ tip of the penis. The levator endopelvic fascia lateral to the ing that organ emerge. Other causes of segmental (spinal) prostate represents the most common location ofTrPs in men facilitation can include stress imposed on a part of the spine with pelvic pain . . . myofascial TrPs were identified and through injury, overactivity, repetitive patterns of use, poor pressure was held for about 60 seconds to release [described posture or structural imbalance (short leg, for example). as myofascial trigger point release technique - MFRT]. Specific physiotherapy techniques used in conjunction with Korr (1978) tells us that when subjects who have had MFRT were voluntary contraction and releaselhold-relax/ facilitated segments identified were exposed to physical, contract-relax/reciprocal inhibition, and deep tissue mobi­ environmental and psychological stimuli similar to those lization, including stripping, strumming, skin rolling and encountered in daily life, the sympathetic responses in effleurage. those segments were exaggerated and prolonged. The dis­ turbed segments behaved as though they were continually The explanation for the success of this approach remains in, or bordering on, a state of 'physiologic alarm'. hypothetical, according to Anderson et al, who have out­ lined possible mechanisms as follows: Therapeutically, any approach that reduces sensory input or interrupts the self-perpetuating activity of that facilitated Pathways in neurogenic inflammation, especially between segment is helpful. Therapeutic intervention can include the central and peripheral nervous and endocrine systems massage, soft-tissue manipulation to relax the muscles, struc­ tural manipulative therapy to mobilize the area, reduction of

6 Trigger points 107 with effects on immunomodulatory mechanisms, will most The protocol of treatment was a s follows: likely provide a pathophysiological explanationfor CPPS. It seems intuitive that central sensitization probably represents 10 intravaginal massages using the Thiele technique by one the basis for hyperalgesia and allodynia in many of these of three qualified women's health nurse practitioners. The men (McCracken & Turk 2002). We must await elucidation technique consisted of massage from origin to insertion of these biochemical pathways and develop an understand­ along the direction of the muscle fibers with an amount of ing of the role ofpro-inflammatory and other cytokines. Our pressure tolerable to the subject. The motion was performed treatment modality is based on the psychophysiological 10 to 15 times during each session to each of the following explanation of painful muscle TrPs being initially activated muscles in order: coccygeus, iliococcygeus, pubococcygeus, by infection, trauma or emotions. Our protocol includes the and obturator internus. At the practitioner 's discretion, 1 0 release of myofascial TrPs, which tends to recreate patient t o 15 seconds ofischemic compression was applied t o trigger symptoms and behavior modification to relax profoundly the points. A typical treatment lasted fewer than 5 minutes. pelvic muscles and modifij the habit offocusing tension in Each massage was scheduled at least 2 days apart to allow the pelvic floor while under stress . . . Our premise is that, in for any inflammation or discomfort from the previous ses­ addition to releasing painful myofascial TrPs, the patient sion to subside. Patients received two massages per weekfor must supply the central nervous system with new informa­ a period of 5 weeks. tion or awareness to progressively quiet the pelvic floor. Interst i t i a l cystitis, dysp a re u n i a a n d sacro i l i a c Interstiti a l cystitis dysfu n cti o n Using similar trigger point deactivation methods, Weiss A link between the sort of symptoms treated in the previous (2001) has reported the successful amel ioration of symp­ examples, as well as dyspareunia (painful intercourse) and toms in patients with interstitial (i.e. 'unexplained') cystitis sacroiliac dysfunction, was noted in a study conducted in using myofascial release. Philadelphia (Lukban et al 2001). Sixteen patients with inter­ stitial cystitis were evaluated (1) for increased pelvic tone and Holzberg et al (2001) showed the effectiveness of trans­ trigger point presence, and (2) sacroiliac dysfunction. The vaginal Theile massage on high-tone pelvic floor muscula­ study reports that in all 16 cases SI joint dysfunction was ture in 90% of patients with interstitial cystitis. Describing identified. Treatment comprised direct myofascial release, the technique, Holzberg et al note: joint mobilization, muscle energy techniques, strengthening, stretching, neuromuscular reeducation and instruction in an Subjects underwent a total of 6 intravaginal massage ses­ extensive home exercise program. The outcome was that sions using the Theile 'stripping technique'. This technique there was a 94% improvement in problems associated with encompasses a deep vaginal massage via a 'back and forth' urination, and 9 of the 16 patients were able to return to pain­ motion over the levator ani, obturator internus, and piri­ free intercourse. The greatest improvement seen is related to formis muscles as well as a myofascial release technique frequency symptoms and suprapubic pain. There was a whereas a trigger point was identified, pressure was heldfor lesser improvement in urinary urgency and nocturia. 8 to 12 seconds and then released. Irrita b l e bowel syn d ro m e As to the mechanisms involved, they report: 'As a result of the close anatomic proximity of the bladder to its muscular A French osteopathic study (Riot et al 2005) investigated a support, it appears that internal vaginal massage can lead new approach to treatment of irritable bowel syndrome to subjective improvement in symptoms of Ie.' (IBS) in which there was a combination of massage of the coccygeus muscle together with physical treatment of fre­ Interstiti a l cystitis and h i g h-to n e pelvic floor quently associated pelvic j oint disorders. One hundred and dysfu n ction one patients (76 female, 25 male, mean age: 54 years) with a diagnosis of levator ani syndrome (LVAS) were studied In a similar study by Holzberg et al (2000) Thiele massage prospectively over 1 year following treatment. Massage was shown to be very helpful in improving irritative blad­ was given with the patient sidelying on the left. Physical der symptoms in patients with interstitial cystitis and high­ treatment of the pelvic joints was given at the end of each tone pelvic floor dysfunction. In addition, it decreased massage session. excessive pelvic floor muscle tone. Patients' symptoms typically included urinary frequency, urgency and pain, Results showed that, of the 101 patients, 47 (46.5%) suffered ranging from mild to incapaCitating in severity. Initially from both LVAS and IBS. On average less than two sessions of all subjects underwent vaginal examination to document treatment were necessary to alleviate symptoms. At 6 months, pelvic floor muscle tenderness (hypertonus) of the coc­ 69% of the patients remained free of LVAS symptoms, while cygeus, iliococcygeus, pubococcygeus, and obturator inter­ 10% still had symptoms but were improved. At 12 months, nus muscles. 62% were still free of symptoms and 10% improved.

1 08 C L I N I CA L APPLI CATI O N O F N E U R O M U S C U LA R TECH N I Q U E S : T H E U PP E R B O DY A similar improvement trend was observed in the IBS LOCAL FAC I LITAT I O N I N MUSCLES patient group (53% IBS-free initially, 78% at 6 months, 72% at 12 months). All 18S-free patients were LVAS-free at 6 months. Baldry (1993) explains: The conclusion was that the LVAS symptoms may be Palpable myofascial bands are electrically silent at rest. cured or alleviated in 72% of the cases at 12 months with However, when such a band is 'plucked' with a finger . . . a one to two sessions, and that since most of 18S patients ben­ transient burst of electrical activity with the same configu­ efited from such treatment, it is logical to suspect a mutual ration as a motor unit's action potentials may be recorded etiology and to screen for LVAS in all such patients. (Dexter & Simons 1981). It is undoubtedly this electrical hyperactivity of motor and sensory nerve fibers at myofas­ What we can learn from these selected examples is tha t cial trigger points that is responsible for the so-called local the influence of active trigger points is to be found beyond twitch response, a transient contraction of muscle fibers the obvious ones of interference in muscle and joint func­ which may be seen orfelt . . . It is also neural hyperirritabil­ tion and the production of pain, and actually extends to vis­ ity which causes both myofascial and non-myofascial trig­ ceral function (bladder and bowels in these examples). It is ger points to be exquisitely tender to touch . . . The amount also clear from the research reported above that mainstream of pressure required to produce this is a measure of the medical scientists are focusing attention on these phenom­ degree of irritability present. ena, and are employing skillfully applied manual method­ ology, such as that outlined in this text, in successfully A similar process of facilitation occurs when particularly treating these conditions. vulnerable sites of muscles (a ttachments, for example) are overused, abused, misused or disused in any of the many H OW TO RECOGN IZE A FACI LITATED S P I N AL ways discussed in Chapter 4. Localized areas of hypertonic­ ity may develop, sometimes accompanied by edema, some­ AREA times with a stringy feel but always with sensitivity to pressure. Many of these tender, sensitive, localized, facili­ A number of observable and palpable signs indicate an area tated areas contain myofascial trigger points, which may, in of segmental (spinal) facilitation. part, derive from this facilita tion process. • Beal (1983) tells us that such an area will usually involve Myofascial trigger points are not only painful themselves two or more segments unless traumatically induced, in when palpated but can also transmit or activate pain (and which case single segments are possible. other) sensations some distance away in 'target' tissues. Leading researchers into pain Melzack & Wall (1988) have • The paraspinal tissues will palpate as rigid or board-like. stated that there are few, if any, chronic pain problems that • With the person supine and the palpating hands under do not have trigger point activity as a major part of the pic­ ture, perhaps not always as a prime cause but almost the paraspinal area to be tested (practitioner standing at always as a maintaining fea ture. Similar to the facilitated the head of the table, for example, and reaching under areas alongside the spine, these trigger points will become the shoulders for the upper thoracic area), any ceiling­ more active when stress, of whatever type, makes adaptive ward 'springing' attempt on these tissues will result in a demands on the body as a whole, not just on the area in distinct lack of elasticity, unlike more normal tissues which they lie. A number of factors that play a role in trig­ above or below the facilitated area (BeaI 1983) . ger point activation and perpetuation are discussed within this chapter. Grieve ( 1986), Gwm & Milbrandt (1978) and Korr (1948) have all helped to define the palpable and visual signs that When a trigger point is mechanically stimulated (by accompany facilitated dysfunction. compression, needling, stretch or other means) it will refer or intensify a referral pattern (usually of pain) to a target • A gooseflesh appearance is observable in facilitated areas zone. An active trigger point refers a pattern that the person when the skin is exposed to cool air, as a result of a facil­ recognizes as being a part of their current symptom picture. itated pilomotor response. When a la tent trigger point is stimulated, it refers a pattern that may be unfamiliar to the person or an old pattern they • A palpable sense of 'drag' is noticeable as a light touch used to have and have not had for a while (previously contact is made across such areas, due to increased sweat active, reverted to latent) (Simons et al 1 999). All the same production resulting from facilitation of the sudomotor characteristics that denote an active trigger point (as reflexes. detailed in this chapter) may be present in the latent trigger point, with the exception of the person's recognition of their • There is likely to be cutaneous hyperesthesia in the related active pain pattern. The same signs as described for seg­ dermatome, as the sensitivity is increased (facilitated). mental facilitation, such as increased hydrosis, a sense of 'drag' on the skin, loss of elasticity, etc., can be observed and • An 'orange peel' appearance is noticeable in the subcuta­ palpated in these localized areas as well. neous tissues when the skin is rolled over the affected segment, because of subcutaneous trophedema. • There is commonly localized spasm of the muscles in a facilitated area, which is palpable segmentally as well as peripherally in the related myotome. This is likely to be accompanied by an enhanced myotatic reflex due to the process of facilitation.

6 Trigger points 1 09 J LOW ERING TH E NEURA L T H R E S H O L D properties) usually minimally present in muscle extracellu­ lar tissue. Electron microscopy showed clusters of platelets There is another way of viewing facilitation processes. One and mast cells discharging mucopolysaccharide-containing of Selye's (1974) most important findings is commonly granules; also shown was increased connective tissue in overlooked when the concurrent impact of multiple stres­ five cases. sors on the system is being considered. Shealy (1984) sum­ marizes as follows. The space-occupying water-retaining substances stretch surrounding tissue, impair oxygen flow, increase acidity Selye has emphasized thefact that any systemic stress elicits and sensitize nociceptors, converting the area into a pain­ an essentially generalized reaction, with release of adrenaline producing trigger point. and glucocorticoids, in addition to any specific damage such stressor may cause. During the stage of resistance (adapta­ Baldry (1 993) refers to questions raised by Awad (1990): tion), a given stressor may trigger less ofan alarm; however, 'Does the accumulation of mucopolysaccharides in . . . these nodules occur as a result of an increased production of this Selye insists that adaptation to one agent is acquired normally occurring substance, or a decrease in degradation, or a change in its quality?' at the expense of resistance to other agents. That is, as one accommodates to a given stressor, other stressors may Awad therefore identifies edema as a part of the etiology require lower thresholds for eliciting the alarm reaction. Of of the trigger point, based on his analysis of the content of considerable importance is Selye's observation that concomi­ the tissue. Non-traumatic reduction of fluid levels and acid­ tant exposure to several stressors elicits an alarm reaction at ity, perhaps involving lymphatic drainage or traditional stress levels that individually are subthreshold. That is, one­ massage techniques, as well as improved oxygenation, third the dose of histamine, one-third the dose of cold, one­ should therefore decrease nociceptive sensitization, some­ third the dose offormaldehyde, elicit an alarm reaction equal thing neuromuscular therapy has as a primary objective. to afill! dose ofany one agent. (Bold italics added) NIM MO'S R E C E PTOR-TONUS TECHNIQU ES In short, therefore, as adaptation to life's stresses and stres­ sors continues, thresholds drop and a lesser load is required [Sch neider et al 200 1 ) to produce responses (pain, etc.) from facilitated structures, whether paraspinal or myofascial. Raymond Nimmo DC (1904-1986) developed an under­ standing of musculoskeletal pain syndromes that paralleled The concept that emotional stress could be one of the fac­ that of Janet Travell (1901-1997), whose work he admired tors was supported by the research of McNulty et al (1994), (Cohen & Gibbons 1998). Nimmo arrived at a different which suggests a mechanism by which emotional factors (from Travell) understanding of the way in which trigger influence muscle pain. Fourteen subjects were evaluated by points (he called these 'noxious generative points') evolve needle electromyography in a trapezius myofascial trigger and of how to treat them. He held to a model in which point and simultaneously in adjacent non-tender trapezius increased muscle tone was the major feature initiating the muscle fibers during a control condition (forward count­ triggers via the effect they had on neural receptors. He saw ing), a stressful condition (mental arithmetic) and resting the trigger as an abnormal reflex arc. baselines. The authors noted: • Excessive levels of muscle tone could result from repeti­ Based on recent data implicating autonomic in nervation in tive or prolonged influence of stressors ('insults'), such as muscle function, we hypothesized that the trigger point cold, trauma, postural strain, etc., acting on them and would be more responsive than the adjacent muscle to psy­ causing projection of impulses through the posterior root chological stress. The results showed increased trigger point to the gray rnatter of the cord. electromyographic activity during stress, whereas the adja­ cent muscle remained electrically silent . . . This may have • Here the highly excitatory internuncial neurons produce significant implications for the psychophysiology of pain a prolonged motor discharge, increasing muscle tone. associated with trigger points. • If there were a 'malfunction' in this feedback system VARYING VIEW POINTS ON TRIGGER POINTS (resulting, Nimmo suggested, from insults such as 'acci­ dents, exposure to cold drafts or from occupations requir­ AWA D ' S ANA LYSIS OF TRIGG ER POINTS ing prolonged periods of postural strain'), hypermyotonia could result, leading to even greater afferent input to the In 1973, Awad examined dissected muscle fascicles (approx­ cord and amplification of additional efferent impulses to imately 1 cm wide and 2 cm long) from muscle 'nodules' . the muscles. Under a light microscope, i n eight o f the 1 0 specimens (dif­ ferent people), large amounts of 'amorphous material' were • This state of abnormally increased tone could become noted between muscle fascicles. This was shown to com­ part of a self-perpetuating cycle, involving involuntary prise acid mucopolysaccharides (with high water-binding sympathetic activity, with reflex 'spillover' causing vaso­ constriction, retention of metabolic wastes and pain. Nimmo's treatment approach was based on releasing the hypertonic status of the muscles ('I found that a proper

1 1 0 CLI N I CA L APPLICATI O N O F N EU RO M U SCU LA R TEC H N I Q U E S : THE UPPER B O DY degree of pressure sequentially applied causes the nervous not intimately related to muscle spasm (Johnson 1 989) . This system to release a hypertonic muscle') (Nimmo 1981). He concept has been strongly encouraged by commercial inter­ called his approach 'receptor-tonus' technique (Nimmo ests in pharmaceutical antispasmodic d rugs. 1957) and it has had a major influence on modern neuro­ muscular therapy (DeLany 1 999). A 1993 review of current Mense et al (2001 ) point out: 'Physiologic studies show chiropractic adj ustive techniques found that just over 40% that muscle pain tends to inhibit, not facilitate, reflex con­ of chiropractors currently utilize Nimmo's approach on a tractile activity of the same muscle.' Even though it may feel regular basis (NBCE 1993). tense, a painful muscle commonly shows no EMC activity. Additionally, not all muscle spasms (as identified by EMC) A series of articles originally published from 1 958 to 1976 are painful. in Nimmo's own newsletter, The Receptor, or in Digest of Chiropractic Economics, was republished as a collection by FIBROTIC SCAR TISSUE H Y POT HESIS Schneider et al (2001). In their text, comments are embed­ ded as footnotes in the original articles in an attempt to Although there may be a few cases where scar tissue is update some material to more current concepts. found within the taut bands of trigger points, scar tissue is not commonly found in biopsies of tender nodules, accord­ IM PROVE D OX YGENAT I ON AND REDUCED ing to Mense et al (2001, p. 261 ). They suggest that if the TrP exists for an extended period of time, chronic fibrotic TRIGGER POINT PAIN - AN E X A M PL E change may eventually evolve; however, this is not pre­ dictable and rapid resolution of the palpable band with spe­ New Zealand physiotherapist Dinah Bradley (1 999), an cific TrP treatment argues against that explanation. expert in breathing rehabilitation, identifies key trigger points in her patients, in the intercostals and upper trapez­ MUSCLE S PINDLE H Y POT HESIS ius as a rule, at the outset of their course of breathing reha­ bilitation. She asks patients to ascribe a value, out of 1 0, to Some theorists oppose the most widely accepted concepts the trigger point when under digital pressure, before they of trigger point formation, those being an integrated commence their exercise and treatment program (during hypothesis, as presented by Simons et al (1999) (discussed which no direct treatment is given to the trigger points more fully below). Hubbard & Berkoff (1993) and Hubbard themselves) and periodically during their course, as well as (1 996) point to a dysfunctional muscle spindle as the source at the time of discharge. of TrP EMC activity. They dismiss the possibility of poten­ tials arising from motor endplates since they believe that Bradley states: the activity is not localized enough to be generated in the endplate, and does not have the expected waveform mor­ I use trigger point testing as an objective measurement. phology nor the expected location. Part of [the patient's] recovery is a reduction in muscu­ loskeletal pain in these overused muscles. I use a numeric Simons et al (1999) and Mense et al (2001 ) both contradict scale to quan tify this. Patients themselves feel the reduction these three assertions, offering a thorough discussion of the in tension and pain, a useful subjective marker for them, location of active loci and their distribution within the end­ and an excellent motivator. plate zone, the nature of spike activity, the lack of concentra­ tion of muscle spindle concentration in the endplate zone This use of trigger points, in which they are not directly where TrPs are found, and current information on wave­ deactivated but are used as monitors of improved breathing form morphology. Additionally, Simons et al (1999, p. 80) function, highlights several key points. give the following four reasons that question the validity of a muscle spindle hypothesis. 1. As breathing function and oxygenation improve, trigger points become less reactive and painful. 1. If the conclusions that these potentials arise from dys­ functional muscle spindles is correct, then Wiederholt's 2. Enhanced breathing function also represents a reduction [1970] comprehensive EMC, histological and pharmaco­ in overall stress, reinforcing the concepts associated with logical study reached an erroneous conclusion and elec­ facilitation - that as stress of whatever kind reduces, trig­ tromyographers ever since have been misled. It may be ger points react less violently. difficult to convince the electromyographic community that what they have identified as endplate potentials are 3. Direct deactivation tactics are not the only way to handle really muscle-spindle potentials . . . trigger points. 2. The presence of action potentials originating at an end­ 4. Trigger points can be seen to be acting as 'alarm' signals, plate that was also the site of a TrP active locus was illus­ virtually quantifying the current levels of adaptive trated [within the cited text] . . . These are motor endplates demand being imposed on the individual. of extrafused fibers. The type of needle used would be mechanically unable to penetrate the capsule of a muscle PAIN-SPAS M - PAIN CYCLE The old concepts of pain-spasm-pain have been aban­ doned due to overwhelming evidence that muscle pain is

6 Trigger points 1 1 1 spindle to reach an intrafusal motor endplate. Muscle excludes the. possibility of a non-muscular origin of the spindles usually lie in loose coTmective tissue. pathology. They suggest that the characteristics of the pain 3. The demonstration that the spikes from a TrP active locus from trigger points are not distinguishablefrom neural pain, can propagate at least 2.6 cm along the taut band pre­ and that a primary neurological cause is a much more likely cludes a muscle-spindle intrafusal-fiber origin. This dis­ explanationfor the local and referred sensations of myofascial tance is twice the total length of a human spindle and four pain. To date, no neurophysiologic studies have confimled or times the half-fiber distance measured in this experiment. denied these claims. Routine nerve conduction testing has not 4. In addition, the clinical effectiveness of Botulinum A identified any abnormalities, but may be lacking the sensitiv­ toxin injection for the treatment of myofascial TrPs sup­ ity to do so. ports the endplate hypothesis. Mense et al (2001) comment on the concepts presented by A further short discussion of EMG needling of trigger GlUU1. (1980) and, more recently, a similar discussion by Chu points is offered later in this chapter. (1995). 'There is much clinical evidence that compression of motor nerves can, at times, activate and perpetuate the pri­ Although discussion of needle penetration methodology, mary TrP dysfunction at the motor endplate. Conversely, TrPs abnormal endplate noise and other associated information are commonly activated by an acute muscle overload that is is beyond the scope of this text, the authors acknowledge its unrelated to a compressive neuropathic process. Neuropathy importance and refer the readers to the above mentioned can be, but is not always, a major activating factor.' work of Simons et al (1999) and Mense et al (2001). RA D ICULOPAT H IC MOD EL FOR MUSCULAR PAIN SIMONS' CURR ENT PERS PECTIV E : AN Some theorists point to a neurological cause as primary and I NT E GRAT E D H Y POT H ESIS trigger points as secondary phenomena (Gunn 1997, Quintner & Cohen 1994). Simons et al (1999) combine two widely accepted theories (energy crisis theory and motor endplate hypothesis) into an Huguenin (2004) explains: integrated hypothesis of trigger point formation. This approach suggests a polymodal model and implies that Gunn (1997) suggested a radiculopathic modelfor muscular there is not a single cause for trigger point formation, but pain and states that 'myofascial pain describes neuropathic rather a cascade of steps that may occur and a variety of pain that presents predominantly in the musculoskeletal sys­ influences that help determine activation and perpetuation. tem' (p. 1 2 1). The radiculopathic model is based on all dener­ vated structures exhibiting super sensitivity. From clinical The energy crisis theory (Bengtsson et a1 1986, Hong 2000, observations, GUHll (1 997) states that neuropathic nerves Simons et al 1999) suggests that trauma, repetitive use or are most commonly found at the rami of segmental nerves, increased neural input (see facilitation discussion earlier in and therefore represent a radiculopathy. If neural injury or this chapter) increases calcium release in the inunediate area compression and partial denervation are the site oforigin of surrounding the motor pOint, resulting in prolonged short­ this pathology, he believes that it helps to explain the lack of ening of the central sarcomeres and the formation of a taut pathology seen in muscle and the sensory, motor, and auto­ band of myofascial tissue. This also results in compromised nomic changes seen in myofascial pain syndromes. circulation (reduced oxygen and nutrients) in the local area with subsequent failure to produce adequate ATP to initiate Gunn (1 997) suggests that myofascial pain most often relaxation of the tissues. As metabolic wastes accumulate, relates to intervertebral disc degeneration with nerve root sensitization of nociceptors occurs as well as direct stimula­ compression or angulation due to reduced intervertebral tion of sensory nerves by pressure from taut tissues. While space and resultant paraspinal muscle spasm. This is this theory is plausible, there are no definitive studies to described as a form of neuropathy. This neuropathy then show that it is the cause of trigger point formation. sensitises structures in the distribution of the nerve root, causes distal muscle spasm, and contributes to other degen­ The motor endplate hypothesis points to the fact that the erative changes in tendons and ligaments within its distri­ motor nerve synapses with a muscle cell at the motor end­ bution that are then perpetuated by the ongoing muscle plate (mid-fiber region in most muscles). Needle EMG studies shortening. Therefore, this theory is not only used to explain (Hubbard & Berkhoff 1993) have found that fibers containing trigger point formation, but also conditions such as trigger points produce characteristic electrical activity (end­ tendinopathy and en thesopathy. plate noise - EPN) when properly measured at the motor end­ plate zone (Simons 2001, Simons et aJ 2002). EPN (previously Based on his theories, Gunn (1 997) proposes that long last­ referred to as spontaneous electrical activity or SEA) (Simons ing pain relief requires needle treatment to the shortened 2004) is thought to represent an increased rate of release of paraspinal muscles in order to reduce nerve root compression, acetylcholine (ACh) from the nerve terminal and to result in as well as to trigger points more local to the site ofperceived action potentials being propagated a small distance along the pain. Quintner & Cohen (1 994) argued that the reasoning muscle cell membrane. This may cause activation of a few behind traditional trigger point teaching is circular and contractile elements, resulting in some degree of muscle shortening (Simons 1996).

1 1 2 CLI N I CA L APPLICATI O N O F N E U RO M U S C U LAR TECH N IQ U E S : T H E U PPER BODY [ C ENTRAL AND ATTACHMENT TRIGGER • Gliding techniques may usefully be applied from the center of the fibers out toward the attachments, unless POINTS contraindicated (as in extremities where vein valves exist). By elongating the tissue toward the attachment, The motor end plate hypothesis can easily coexist with the sarcomeres that are shortened at the center of the fiber energy crisis theory and together comprise the integrated will be lengthened and those that are overstretched near hypothesis as presented by Simons et al ( 1999). Based on the attachment sites will have the tension released. this concept, they see the strong need to differentiate 'cen­ tral' from 'attachment' trigger points, both in their nature • Central trigger points often respond well to heat as and in treatment requirements. The following highlights warmth may encourage the gel of the fascia to turn more critical pOints to consider when applying therapy to trigger solute (Kurz 1 986) . Heat draws fresh blood to the area, points. Much of this information is discussed at length in bringing with it oxygenation and nutrients. Subsequent Myofascial Pain and Dysfunction: The Trigger Point Manual, val l, application of cold (see below and Chapter 10) or mas­ 2nd edn. sage is required to prevent stasis and congestion follow­ ing application of heat. • Central trigger points (CTrPs) are usually directly in the center of a fiber's belly. • Short (20-30 seconds) cold applications, once removed, produce a strong flushing of the tissues (Boyle & Saine • Motor points are consistently located (with a few excep­ 1988). Cold applications are likely to penetrate to deeper tions) in the center of the muscle fiber 's belly. tissue than heat (Charkoudian 2003) although prolonged, continuous applications of ice may decrease the pliability • The practitioner who knows fiber arrangement (fusiform, of connective tissue so that they are less easily stretched pennate, bipennate, multipennate, etc.), as well as attach­ (Lowe 1995). ment sites of each tissue being examined, will find it easy to locate the triggers since their sites are moderately pre­ • Oxygen, ATP and nutrients offered by the incoming dictable (see Fig. 2 .6, p. 28) . blood could reduce the local environmental deficits and encourage normalization of the dysfunctional tissues. • A ttachment trigger points (ATrPs) develop where fibers merge into tendons or at periosteal insertions. • When compression techniques are used, local chemistry can change due to blanching of the nodules followed by • Tension from taut bands on periosteal, connective or a flush of blood to the tissues when the compression is tendinous tissues can lead to enthesopathy or enthesitis, released. disease processes where recurring concentrations of muscular stress provoke inflammation with a strong ten­ • The effects of thermal or other neuro-altering applica­ dency toward the evolution of fibrosis and the deposition tions (skin irritants, moxibustion, dry or wet needling, of calcium. etc.) may induce the contracture to release more readily. • Both central and attachment trigger points can have the PRIMARY, K EY AND SATELLITE same end result - referred pain. However, the local processes, according to Simons et ai, are very different TRIGGER POINTS and should be addressed differently. A primary TrP is a central TrP that was directly activated by • Central trigger points would be treated with their con­ acute or chronic overload, or by repetitive overuse of the tracted central sarcomeres and local ischemia in mind. muscle in which it is housed. It was not activated by TrP activity in another muscle. Appropriate and successful treat­ • Until they are thoroughly examined and tissue reaction ment of a primary trigger point relieves its associated refer­ noted, attachment trigger points should be treated with ral pattern. their tendency toward inflamam tion in mind. For exam­ ple, ice applications would be more appropriate than KeJl TrPs and satellite TrPs are related. Clinical experience heat in areas where enthesitis is suspected. and research evidence suggest that a key TrP is one that is responsible for the development and activity of one or more • Since the end of the taut band is likely to create enthe­ satellite TrPs. A satellite TrP can be located within the target sopathy, stretching the muscle before releasing its central area of the key TrP. However, it can also be housed in a syn­ trigger point might further inflame the attachments. ergist, in an antagonist or in a muscle linked neurogenically to the key TrP. When a key TrP is deactivated, this also deac­ • Therefore, it is suggested, the attachment trigger points tivates its satellite TrP(s) and relieves the satellite's associ­ should first be addressed by releasing the associated cen­ ated referral pattern. If these key TrPs are not deactivated, tral trigger point. and only the satellites are treated, the referral pattern usu­ ally returns. The identification of a TrP as a 'key' is • Stretches, particularly involving active ranges of motion, confirmed when deactivation of it also deactivates the sat­ will then further elongate the fibers but should be ellite TrP. Distinguishing a key from a satellite is rarely applied mildly until reaction is noted so as to avoid fur­ accomplished by examination alone. In fact, unless the ther tissue insult. • When passive stretching is applied, care should be taken to assess for tendinous or periosteal inflarrunation, avoid­ ing increased tension on al ready distressed connective tissue attachments.

6 Trigger points 1 1 3 practi tioner stays ever mindful of the existence of this rela­ Box 6.3 Trigger point activating factors tionship, successful reduction of TrP referral patterns can be thwarted. Primary activating factors i nclude: Key TrPs are primary TrPs, but not all primary TrPs • persistent m uscu la r contraction, strai n or overuse (emotional become key TrPs. Satellite TrPs are not primary TrPs since or physical cause) they develop associated with a key TrP, and not as a result of d irect activation by overload or overuse. • trauma (local inflammatory reaction) • adverse environmental conditions (cold, heat, damp, draughts, Hong & Simons (1992) have reported on over 100 sites involving 75 patients in whom remote trigger points were etc.) inactivated by means of injection of key triggers. The details • prolonged immobility of the key and satellite triggers, as observed in this study, • febri le i l l n ess are listed below. • systemic biochemical i mbalance (e.g. hormonal, n utritional). Key trigger Satell ite triggers Secondary activating factors include (Baldry 1 993): Sternocleidomastoid Upper trapezius Temporalis, masseter, d igastric • compensating synergist and antagonist muscles to those housing primary triggers may develop triggers Sca l e n i i Temporalis, masseter, splenius, semispinal is, levator scapu lae, rhomboid • sate l l ite triggers evolve i n referral zone (from pri mary triggers Splenius capitis major or visceral disease referral, e.g. myocardial infarct). Supraspinatus I n frasp inatus Deltoid, extensor carpi radialis, extensor attachment site, and is true whether it is a primary, key or Pectora l is m i nor digitorum communis, extensor carpi satellite. However, its state of being 'turned on', that is, part of Latissimus dorsi ulnaris the person's consistent pain (or other sensation) experience is Serratus post. su p. determined by its active or latent status. Tempora lis, semispi nalis Deep paraspinals (L5-S1 ) The terms active and latent apply to the person's recogni­ Deltoid, extensor carpi radialis tion of, or familiarity, with the referred pa ttern. An active TrP Quadratus l u m borum and a latent TrP are the same in almost every way, except for Piriformis Biceps brachii the person's recognition of the pattern as part of their com­ Hamstrings plaint (clinical symptoms) . If, when a TrP is stimulated, the Flexor carpi radial is, flexor carpi ulnaris, person recognizes the pattern of referral, then it is classified first dorsal interosseous as active. H, instead, the person is not familiar with that sen­ sation, it is classified as latent. A latent trigger point other­ Triceps, flexor carpi ulnaris wise has all the same capabilities as an active trigger point, including the ability to affect the tissues in its target zone on Triceps, latissimus dorsi, extensor an ongoing basis, even though it is clinically quiescent. It can d ig itorum com m u n is, extensor carpi be compared to an electrical switch for a light fixture. It is in ulnaris, flexor carpi ulnaris place, ready to illuminate, but lUltil the switch is 'turned on' the person is unaware of its existence. When a latent TrP Gluteus maxim us, medius and m i n i m us, becomes activated, the person may be as surprised as if a piriformis, hamstrings, tibialis, peroneus light were suddenly turned on in a dark room. Like the longus, gastrocnemius, soleus switch for the light, a latent trigger point is already fully developed and only needs an activating circumstance (i.e. Gluteus maximus, med ius and m i n i m us, additional stress) to make its associated referral pattern pi riformis become one of the person's common complaints. Ha mstri ngs Recent research (Shah et al 2003, 2005) has revealed that concentrations of chemicals, including substance P, calcitonin Peroneus longus, gastrocnemius, soleus gene-related peptide (CGRP), bradykinin, norepinephrine and others, are present at the nidus of trigger points when ACTIVE AND LATE N T TRIGGER POINTS compared to normal tissue. Additionally, increased levels of these substances, as well as lower pH (i.e. a more acid envi­ A trigger point, by definition, is a tender palpable nodule ronment), were noted in active TrPs when compared to latent within a taut band, that when provoked refers a sensation trigger points. Regarding the findings of this research, (usually pain) to its associated target zone. It may also prevent Simons (2006) comments: full range of motion of the muscle in which it is housed, pro­ duce a twitch response when properly provoked, and pro­ Remarkably, and unexpectedly, the clinical distinction duce referred motor and/ or autonomic phenomena and / or between active and latent MTrPs was sharply distinguished tenderness within its target zone. This is true, whether the by the concentration of these stimulants of nociception. It is trigger point develops in the center of the fibers or at an becoming apparent that the active MTrPs are specifically associated with the referred and local pain characteristics of

1 1 4 C LI N I CA 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 TR I G G ER POINTS ASSOCIAT E D W I T H SHOU L D ER RESTRICTION ( K u c h e ra Et M c Pa rt l a n d 1 9 9 7 ) • Active trigger points, when pressure is applied to them, refer a Restricted motion M u scle housing trigger point pattern that is recognizable to the person, whether pain, tin­ Flexion g l ing, n u mbness, burning, itching or other sensation. Abduction Triceps • Latent trigger poi n ts, when pressure is applied to them, refer a Internal rotation S u bsca p u l a r i s pattern that is not fa m i l iar or perhaps one that the person External rotation I nfraspinatus used to have in the past but has not experienced recently. Supraspinatus Teres major • Latent trigger points may become active trigger points at any Levator scapu lae time, perhaps becoming a 'common, everyday headache' or adding to or expanding the pattern of pain being experienced. Teres major I n fraspinatus • Activation may occur when the tissue is overused, stra i ned by overload, chil led, stretched (particu larly abruptly). shortened, Subscapularis traumatized (as i n a motor vehicle accident or a fa ll or blow) Pectoralis minor or when other perpetuating factors (such as poor nutrition or shallow breathing) provide less than optimal conditions of tissue health. • Active trigger poin ts may become latent trigger poin ts with their referral patterns subsiding for brief or prolonged periods of t i m e. They may then become reactivated with their referral patterns retu rning for no apparent reason, a condition that may confuse the practitioner as well as the person. MTrPs while the motor effects are commonly associated OT H ER TRIG G ER POINT SIT ES with latent MTrPs. It is now clear that clinicians need to distinguish these two kinds of MTrPs in their examination Trigger points may form i.n numerous body tissues; how­ ofpatients with musculoskeletal dysfunctions. ever, only those occurring in myofascial structures are named 'myofascial trigger points'. Non-myofascial trigger ESSENTIAL AND S PILLOVER TARGET ZONES points may also occur in skin, fascia, ligaments, joints, cap­ sules and periostiwn (Mense et al 2001 ). Trigger points are associated with a conunon target zone of referral. An essential pattern of referral (usually drawn darker Trigger points often develop in scar tissue (Mense et al in most illustrations of target zones) is one that is present in 200 1, Simons et a1 1999) and may perpetuate the original pain almost every patient presenting with that active trigger pattern, even after the original cause of the pain has been point. A spillover zone includes other regions to which the removed . Additionally, the scar tissue might block normal trigger point may a lso refer in some, but not all, patients, lymphatic drainage (Chikly 1996, 2001), which results in a depending upon the hyperirritability of the trigger point. It is build-up of waste products in surrounding tissue and may important to understand that the spillover region can be encourage trigger point formation or recurrence. every bit as intense as the essential pattern. The darker color in the graphic (essential pattern) is not relevant to intensity, Somatic dysfunction can be caused by visceral referral only with commonality of the reported pattern. A person (Chaitow & DeLany 2003) with evidence of mediation at the may report any, or all, of the target zone, with degrees of level of the spinal cord (O'Connell 2003). Somatovisceral intensity varying from person to person and even from day referrals could be silent, as organs do not always report to day within the same person. pain; however, recurrent viscerosomatic referrals (low back pain) could be an organ's painful cry for help (kidney stone, TRIGGER POINTS AND JOINT RESTRICTION infection or disease) (see Chapter 4 and Fig. 6.5). Although viscerosomatic referrals, such as the arm pain often experi­ (Ku c h e ra & M c Pa rt l a n d 1 997) enced with a myocardial infarction, are conunonly noted for most organs (Mense et al 2001), they often represent life­ Since trigger points can influence their associated synergis­ threa tening underlying root causes. Specific diagnosis of tic and antagonistic m uscles and are associated with loss of visceral pain is therefore mandatory and referral to the range of motion of the tissue housing them, all muscles appropriate practitioner for prompt evaluation should not associated with a joint suffering a restriction of movement be delayed. should be examined for trigger point involvement. Though this may occur at any jOint, the following example is given TESTING AND MEASURING TRIGGER POINTS for the shoulder region, as noted by Kuchera. As the trigger point phenomenon continues to attract high levels of research interest, it becomes increasingly impor­ tant for standardized criteria to be established relating to

Left eye Upper molars Upper molars 6 Trigger points 1 1 5 =::J Side of tongue Left lower molars Pharynx and larynx Tip of tongue Heart Central portion Right eye of left diaphragm Right Pharynx and larynx Diaphragmatic Right lower diaphragm pericardium molars (central portion) Stomach and Left lung and Pleura pancreas pleura (C3-T 1 2) Heart liver Pleura Central portion of Spleen Pancreas Gallbladder and Heart right diaphragm duodenum Gastrojejunal Appendix (ulcer) Spleen Cancer of esophagus Heart and aortic aneurysm Renal pelvis Rectum and trigone Mesentery and and ureter region of bladder Gallbladder intestines Heart Right ovary Bladder fundus and tube Right kidney Bladder trigone and renal pelvis Uterine cervix AB F i g u re 6.S Pai n referred from viscera. A : Anterior view. B : Posterior view. Adapted from Rothstein et al ( 1 99 1 ) . the skills required to identify and treat myofascial dysfunc­ Practitioners should be able to identify: tion. To date, no definitive, reliable method of imaging trig­ ger points or laboratory test is available to assist in the • bony structures diagnosis of a trigger point (Simons 2004). Manual palpa­ • individual muscles (where possible) tion and physical examination, combined with a thorough • palpable thickenings, bands and nodules within the case history, remains the diagnostic standard. myofascial tissues. BAS IC S KILL REQUIREMENTS Additionally, knowledge of fiber arrangement and the short­ ened and stretched positions for each section of each muscle When designing and conducting clinical studies relating to will allow the practitioner to apply the techniques in such a soft tissue dysfunction, it is important that the examiners be way as to obtain accurate and reliable results. Knowledge of experienced and well trained in those palpation skills and (or accessible charts showing) trigger point reference zones protocols required to accurately assess the tissues. Those will offer greater accuracy. who are inexperienced (recent graduates or students, for example) or experienced practitioners with insufficient Simons et al (1 999) discuss diagnostic criteria for identi­ training in the specific techniques required may well fall fying a trigger point: short of the skills needed to apply technique-sensitive strategies. This is especially true of those applying manual • taut palpable band techniques, since palpa tion skills take time and practice to • exquisite spot tenderness of a nodule in the taut band perfect. Experienced practitioners who are trained to pal­ • recognizable referral pattern (usually pain) by pressure pate for, and identify, specific characteristics that form part of research criteria (see below) will offer the most useful on a tender nodule (active with familiar referral or latent and valid findings (Simons et aI 1999). with unfamiliar referral) • painful limit to full stretch range of motion.

1 1 6 C L I N ICAL A P P L I CAT I O N O F N EU R O M USCU LAR TECH N I Q U E S : T H E U P PER B O DY L Additional observations: • the recording of both high-amplitude spike potentials and low-amplitude noise-like components • local twitch responses (LTRs) identified visually, tactilely or by needle penetration • the belief system of the operator as to what 'normal end­ plate noise' represents. • altered sensations in reference zones • electromyographic verification of spontaneous electrical Simons et al (1999) state: activity (SEA) found in active loci of trigger point. The issue ofwhether the endplate potentials now recognized by electromyographers as endplate noise arise from normal Identification of a local twitch response is the most difficult; or abnormal endplates is critical and questions conventional however, when it is present, it supports a strong confirma­ belief . . . Since publication of the paper by Wiederholt in tion that a trigger point has been located, especially when 1970, electromyographers have accepted his apparently mis­ elicited by needle penetration. Additionally, pain upon con­ taken conclusion that potentials similar to what we now traction and weakness in the muscle may be observed. identify as SEA [spontaneous electrical activity] represent normal miniature endplate potentials. Given the above criteria and the fact that no particular laboratory test or imaging technique has been officially Electromyographers commonly identify the low-ampli­ established to identify trigger points (Simons et aI 1 999), the tude potentials as 'seashell' noise. Wiederholt was correct in development of palpation skills is even more important. concluding that the low-amplitude potentials arose from Additionally, several testing procedures may be used as endplates, and illustrated one recording of a fe<.I.! discrete confirmatory evidence of the presence of a trigger point monophasic potentials having the configuration of normal when coupled with the above minimal criteria. miniature endplate potentials as described by physiologists. However, the continuous noise-like endplate potentials that NE E DLE EL ECTROMYOGRA P H Y he also illustrated and that we observefrom active loci have an entirely difef rent configuration and have an abnormal While this method o f testing would not be practical i n most origin . practice settings, the obvious value in clinical research is high. Though a thorough discussion of this material is Advancing the penetrating needle very slowly and with beyond the scope of this text, the reader is referred to Simons gentle rotation is a key factor in arriving at the active loci et al (1999) who have extensively discussed spontaneous without provoking an insertion-induced potential which electrical activity, needle penetration methodology, abnormal could distort the noise produced by the dysfunctional end­ endplate noise and other associated information that has plate. Simons et al (1999) note: only been briefly discussed here. As the needle advances through the TrF region in this elec­ The above-mentioned text offers evidence of the impor­ tronically quiet background, the examiner occasionally tance of several factors when using EMG needling for trig­ hears a distant rumble of noise that swells to full SEA ger point diagnosis. They include: dimensions as the needle continues to advance. Sometimes the SEA can be increased or decreased by simply • the type and size of needle used to penetrate the trigger applying gentle side pressure to the hub of the EMC needle. point The distance of the needle from the discrete source of the electrical activity can be that critical. • the speed and manner in which the needle is inserted • the sweep speed used for recording 1 . 200 asymptomatic Air Force recruits aged 1 7-35 demon­ ULTRASOUND strated trigger points in 54% of 100 females and 45% of 100 males tested (Sola et al 1 951). Visual imaging of the local twitch response (LTR) provides objective evidence tha t an LTR has been provoked. While it 2 . Triggers c a n occur i n a n y myofascial tissue but the most com­ may be clinically practical to use ultrasound, the practitioner monly identified trigger points are found i n the u pper trapez­ would still need to provoke the LTR. This would involve nee­ ius and quadratus lumborum (Travel l Et Simons 1 983b). ('A dle penetration or the development of snapping palpation latent trigger point in the third finger extensor may be more skills . Snapping palpation is a difficult technique to master common' Simons et al 1 999.) and is not applicable to many of the muscles. However, when it is possible to do so, this method provides non-invasive 3. I ncidence of primary myofascial syndromes noted in 85% of supporting evidence that a trigger point has been found. 283 consecutive chronic pain patients and 55% of 1 64 chronic head/neck pain patients (Fishba i n et al 1 986, Fricton SURFACE EL ECTRO MYOGRA P H Y et al 1 985). Surface EMG offers a promising possibility o f studying the 4. Most common trigger point sites are : effects that trigger points have on referred inhibition and • belly of muscle, close to motor point • close to attachments • free borders of m uscle.

6 Trigger points 1 1 7 referred spasm to other muscles. With well-designed stud­ takes more than 4 kg of pressure to produce pain, the point does not count in the tally. Without a measuring device, such ies, this may provide evidence that trigger points increase as an algometer, there would be no means of standardizing pressure application. An algometer is also a useful tool for responsiveness and fatigability and dela. y recovery of the training a practitioner to apply a standardized degree of pres­ muscle. sure when treating and to 'know' how hard they are pressing. ALGOMETER USE FOR RESEARC H AND CLINICAL Use of a hand-held algometer is not really practical in everyday clinical work but this becomes an important tool if TRAINING research is being carried out, as an objective measurement of a change in the degree of pressure required to produce symp­ When applying digital pressure to a tender point in order to toms. The research by Hong and colleagues as to 'which ascertain its status (Does it hurt? Does it refer? etc.), it is treatment method is most successful in treating trigger important to have some way of knowing that pressure being points' reported on later in this chapter, utilized algometer applied is Wliform. The term 'pressure threshold' is used to readings before and after treatment and could not usefully describe the least amount of pressure required to produce a have been carried out without such an instrument. report of pain and / or referred symptoms. It is obviously useful to know whether pain and /or referral symptoms An electronic algometer that fits over the thumb allows occur with 1, 2, 3 or however many kilograms of pressure recording of pressures applied to obtain feedback from the and whether this degree of pressure changes before and patient and to register the pressure being used when pain after treatment or at a subsequent clinical encOlmter. levels reach tolerance. A lead from the algometer connects to a computer, giving precise readouts of the amount of In diagnosing fibromyalgia, the criteria for a diagnosis pressure being applied during assessment or treatment depend upon 11 of 18 specific test sites testing as positive (Fryer & Hodgson 2005) (Figs 6.7 and 6.8). (hurting severely) on application of 4 kg of pressure (American College of Rheumatologists 1990) (Fig. 6.6). If it • Va rious stud ies have demonstrated that trigger po ints in one T H ER MOGRA P H Y AND TRIGGER POINTS muscle are related to in hibition of another functionally related muscle (Simons 1 993b). Various forms of thermography are being used to identify trigger point activity, including infrared, electrical and liq­ • In particular. it was shown by Simons that the deltoid m uscle uid crystal (Baldry 1993). Swerdlow & Dieter ( 1992) found, can be inhibited when there are i nfraspinatus trigger points after examining 365 patients with demonstrable trigger present. points in the upper back, that 'Although thermographic \"hot-spots\" are present in the majori ty, the sites are not nec­ • Head ley ( 1 993) has shown that lower trapezius i n h i bition is essarily where the trigger poin ts are located.' Their study related to trigger points in the upper trapezius. Figu re 6.6 ARB: N i n e pa i rs of poi nts used in testing for fibromyalgia. Reproduced with permission from Chaitow (1 996b).

1 1 8 CLI N I CA L APPLICATI O N O F N EU RO M USCULAR TECH N I QUES: T H E UPPER BODY [ this anomaly to the different effects trigger points have on the autonomic nervous system. Simons (1993a) explains: Depending upon the degree and manner in which the trig­ ger point is modulating sympathetic control of skin circula­ tion, the reference zone initially may be warmer, isothennic or cooler than unaffected skin. Painful pressure on the trig­ ger point consistently and significantly reduced the temper­ ature in the region of the referred pain and beyond. Barrell (1996) has shown that manual-thermal diagnosis is only accurate regarding what the hand perceives as 'heat' 70% of the time. Apparently when scanning manually for heat, any area that is markedly different from surrounding tissues in temperature terms is considered 'hot' by the brain. Manual scanning for heat is therefore an accurate way of assessing 'difference' between tissues but not their actual thermal status. F i gure 6 . 7 Digital algomete r (pl iances capacitance sensor) attached CLI NICAL F EATUR ES OF MYO FASCIAL to the thumb. Rep roduced with p ermission from the Journal of TRI G G ER POINTS (Kuchera Et McPartland 1997) Bodywork and Movemen t Therapies 9 (4) :248-255. Simons et al (1999) have detailed recommended criteria for identifying a latent or active trigger point. They note all trigger points as having four essential characteristics and a number of possible confirmatory observations, which may or may not be present. 'Clearly, there is no one diagnostic examination that alone is a sa tisfactory criterion for routine clinical identification of a trigger point . . . The minimum acceptable criteria is the combination of spot tenderness in a palpable band and subject recognition of the pain.' The four essential characteristics of active and latent trig­ ger points are: Figure 6.8 Manual pressure release. Rep roduced with permission • taut, palpable band • small nodular or spindle-shaped thickening in the fiber's from the Journal of Bodywork and Movement Th erapies center which is exquisitely tender when pressed (also 9(4) :248-255. called 'nidus' or 'active loci') • person's recognition of current pain complaint (active TrP) or of an unfamiliar one (latent TrP) when the trigger point is mechanically stimulated • painful limit of stretch range of motion. Other common characteristics of active trigger points include: suggests that while hot-spots may commonly represent • local twitch response (LTR) is seen (visually or by ultra­ trigger point sites, some triggers may exist in 'normal' tem­ sound) or felt as taut band is snapped or nodule is pene­ pera ture regions and hot-spots can exist for reasons other trated by a needle (both techniques are difficult to perform than the presence of trigger points. and require a high level of skill) Thermal examination of the reference zone (target area) • compression of tender nodule produces pain or altered may show skin tempera ture raised but it may become sensation in the target zone hypothermic when the associated trigger point is com­ pressed (Simons et al 1999, p. 30). Simons (1987) attributes • EMG evidence of SEA in active loci • painful upon contraction • muscle weakness.

6 Trigger points 1 1 9 Travell Et Simons ( 1 983a, 1 992) confirm that the fol lowing Boggy local tissue Temperature stressors help to maintain and enhance trigger point activity: Cutaneous humidity differs from increased over surrounding • nutritional deficiency (especial ly vitamins C, B-complex and myofascial point tissues i ron) Skin adheres =--= Skin displays • hormonal imbalances (thyroid in particular) more tightly reduced • infections to underlying elasticity • allergies (wheat and dairy, in particular) fascia ---,. • low oxygenation of tissues (aggravated by tension, stress, Direction inactivity, poor respiration). of eliciting palpation ---. Taut band---\",'C (ir--+Taut band Relaxed containing muscle trigger point fibers --'- Taut bands seem to represent areas in which : Local twitch • muscle fibers in circu mscribed areas seem to be undergoing physiological contracture of taut band • sarcoplasmic reticulum may have been 'damaged', releasing Fig u re 6.9 A l te red physiology of tissues in reg ion of myofascial ca lcium ions and activating actin-myosin contractile mecha­ trigger point. nisms in contiguous muscle fiber sarcomeres • Compressions may be applied wherever the tissue may • there is evolution of ischemia and accu mulation of metabo­ be lifted without compressing neurovascular bundles. lites, which leads to persistent vasoconstriction reflex response • A general thickening in the central portion of the mus­ cle's belly will usually soften or lessen in size when a • depletion ofATP prevents calcium from being returned to broad general pressure is applied by using a broad, pin­ repository, so maintain ing sarcomere shortening cer compression (finger pads). • there are other factors yet to be identified which maintain • A more specific compression of individual fibers is possi­ ca lcium concentrations. ble by using the more precise pincer compression using the tips of the digits or by using flat palpation against Other palpable signs have been observed by the authors of underlying structures, both of which methods entrap this text and others. These include: specific bands of tissue. • altered cutaneous temperature (increased or decreased) • The presence of underlying structures, including neu­ • altered cutaneous humidity (usually increased) rovascular courses that might be impinged or com­ • altered cutaneous texture (sandpaper-like quality, rough­ pressed and sharp surfaces such as foraminal gutters, will determine whether pincer compression or flat palpa­ ness) tion is appropriate. Sometimes either can be used (see • a 'jump' sign (or exclamation! ) may accompany palpa­ Figs 9.3 and 9.4). tion due to extreme sensitivity • Compression techniques between fingers and thumb • local trophic changes or 'gooseflesh' may be evident have the advantage of offering information from two or more of the examiner's digits simultaneously, whereas overlying trigger site or in target zone. flat palpation against underlying tissues offers a more solid and stable background against which to assess the D EVELOPING SKILLS FOR T r P PALPATION tissue. The following suggestions will help develop or refine pal­ • Additionally, the tissue can be rolled between fingers and pation skills that are needed to locate and deactivate trigger thumb to assess quality, density, fluidity and other char­ points. While these points are generalized, advice regarding acteristics that may offer information to the discerning specific examination of individual muscles is offered in the touch. second half of this text dealing with clinical applications of NMT. • Tendons should be accounted for when looking for cen­ tral trigger points with the fiber's actual length being the • Central trigger points are usually palpable either with focus. For example, the tendon of either biceps brachii flat palpation (against underlying structures) or with head is not included when assessing for central trigger pincer compression (tissue held more precisely between points in this muscle. Only the length of the belly of the thumb and fingers like a C-clamp or held more broadly, with fingers extended like a clothes pin) (see hand posi­ tions, Chapter 9, Fig. 9.4).

1 20 C L I N ICAL APPLICATIO N O F N E U R O M U SCULAR TEC H N I QU E S : THE U PPER B O DY [ \\\\--.1\\/ I • Diarrhea, dysmenorrhea t • Diminished gastric motility • Vasoconstriction and headache I� • Dermatographia j'l\\ • Proprioceptive d isturbance, d izziness • Excessive maxillary sinus secretion � • Loca l ized sweating • Cardiac a rrhythmias (especia l ly pectora l is major triggers) F i g u re 6. 1 0 Testi n g skin a n d fascial m o b i l ity bi laterally as loca l • Gooseflesh tissues a re taken toward the e lastic e n d of ra nge. • Ptosis, excessive lacrimation • Conjunctival reddening as inflammation and ischemia. Trigger point activity is likely in areas of greatest 'difference' Box • movement of skin on fascia - resistance to easy gliding of skin on fascia indicates general locality of reflexogenic Travell Et Simons ( 1 983a) have identified triggers that impede activity, i.e. possible trigger point (Lewit 1992), and can lymphatic function. indicate lymphatic congestion which may be contribut­ ing to the etiology • The sca lenes (anterior, i n particular) can ent ra p structures • local loss of skin elasticity - can refine localiza tion of site passing through the thoracic inlet. of trigger poin ts, as can ex tremely light single-digit stroking, which seeks to locate a 'drag' sensation (evi­ • This is aggravated by 1 st rib (a nd clavicu lar) restriction (which dence of increased hydrosis in and under the skin), can be caused by triggers in a nterior and middle scalenes). which offers pinpoint accuracy of location • digital pressure (angled rather than perpendicular) into • Scalene trigger points have been shown to reflexively suppress the suspected tissues seeks confirmation of active trigger lymphatic duct peristaltic contractions in the affected or latent trigger points (Kuchera & McPartland 1997). e x t r e m i ty. Trigger point deactivation possibilities, which will be exam­ • Triggers i n the posterior axil lary folds (subscapularis, teres ined in later sections of this book, include (Chaitow 1996b, major, latissimus dorsi) i nfluence lymphatic d ra inage affecting Kuchera & McPartland 1997): upper extremities and breasts (Travel l Et Simons 1 992). Similarly, triggers i n the anterior axillary fol d (pectoralis • inhibitory soft tissue techniques (previously called m i nor) can be implicated i n lymphatic dysfu nction affecti ng ischemic compression, now referred to as trigger point the breasts (link 1 981). pressure release) including neuromuscular therapy! massage muscle is considered, which places the predictable zone of central trigger point location much further distally on • chilling techniques (cryospray, ice) the upper arm than it would be if the tendons were • acupuncture, injection, etc. (dry or wet needling) included. • positional release methods • Muscles with tendinous inscriptions (tendinous bands • muscle energy (stretch) techniques (including both pas­ traversing muscles which divide them into sections, such as occurs in rectus abdominis) will have an endplate sive and active forms of isometric contraction) zone within each section. • The fiber arrangement of all underlying and overlying tissues should be considered when approaching layers of muscles with manual assessment so as to include all of them. Additional palpation skills may be used to discover the presence of trigger points, facilitated tissue and myofascial restrictions (Figs 6.10 and 6.11). These skills require practice before accuracy is reliable; however, once developed, they are clinically valuable. They include (Chaitow 1996a): • off-body scan (manual thermal diagnosis); which offers evidence of variations in local circulation, probably resulting from variations in tone, as well as factors s uch

6 Trigger points 1 2 1 A used approaches as well as a placebo treatment (Hong et al 1993). The methods included: Figure 6. 1 1 ARB : Skin elasticity is evaluated by stretchi n g apart to 1. ice spray and stretch (Travell & Simons approach) the e l astic barrier and comparing with the ran g e of the surrounding 2. superficial heat applied by a hydrocolator pack (20-30 ski n . minutes) • myofascial release methods 3. deep heat applied by ultrasound (1 .2-1 .5 watt/cm2 for 5 • combination sequences such as integrated neuromuscu­ minutes) lar inhibition technique (INIT; Chapter 9) 4. dummy ultrasound (0.O watt/cm2) • correction of associated somatic dysfunction possibly 5. deep inhibitory pressure soft tissue massage (10-15 min­ involving high-velocity thrust (HVT) adjustments and/ or utes of modified connective tissue massage and shiatsu/ ischemic compression). osteopathic or chiropractic mobilization methods • education and correction of contributory and perpetuat­ Eighty-four patients were selected who had active triggers in the upper trapezius which had been present for not less ing factors (posture, diet, stress, habits, e tc.) than 3 months and who had had no previous treatment for • self-help strategies (stretching, hydrotherapy methods, these for at least 1 month prior to the study (as well as no cervical radiculopathy or myelopa thy, disc or degenerative etc.). disease). Twenty-four normal subjects were included. W H IC H MET H O D I S MORE EFFECT I VE ? • The pain threshold of the trigger point area was meas­ ured using a pressure algometer three times pretreat­ Researchers at the Department o f Physical Medicine and ment and within 2 minutes of treatment . Rehabilitation, University of California, Irvine, evaluated the immediate benefits of treating an active trigger point in • The average was recorded on each occasion. the upper trapezius muscle by comparing four commonly • A control group was similarly measured twice (30 min­ u tes apart) who received no treatment until after the sec­ ond measurement. • The results showed that all methods (but not the placebo ultrasound) produced a significant increase in pain threshold following treatment, with the greatest change being demonstrated by those receiving deep pressure treatment (which equates with the methods advocated in neuromuscular therapy). • The spray and stretch method was the next most efficient in achieving increase in pain threshold. The researchers suggest that: Perhaps deep pressure massage, if done appropriately, can offer better stretching ofthe taut bands of musclefibers than manual stretching because it applies stronger pressure to a relatively small area compared to the gross stretching of the whole m uscle. Deep pressure may also offer ischemic com­ pression which [has been shown to be] effective for myofas­ cial pain therapy. (Simons 1 989) Hou et al (2002) conducted further investigation as to appli­ cation of ischemic compression ( trigger point pressure release) in combination with a variety of o ther modalities. They concluded that: Ischemic compression therapy provides alternative treat­ ments using either low pressure (pain threshold) and a long duration (90s) or high pressure (the average of pain thresh­ old and pain tolerance) and short duration (30s) for imme­ diate pain relief and MTrP sensitivity suppression. Results suggest that therapeutic combinations such as hot pack plus active ROM and stretch with spray, hot pack plus active ROM and stretch with spray as well as TENS, and hot pack

1 22 C L I N I CA L APPLICATI O N O F N EU R O M USCULAR TEC H N IQUES: T H E U PPER B O DY plus active ROM and interferential current as well as can powerfully release the contractures and teach the person myofascial release technique, are most effective for easing new skills for maintaining the release. Little long-tenn bene­ MTrP pain and increasing cervical ROM. fit is derived from the mechanical release alone. At-home stretches, changes in usage and a ttention to other perpetuat­ When precise palpation and release techniques are combined ing factors will alter the conditions that have helped build the with elongation of the tissues (stretching), the combination trigger points and help prevent them from recurring. Refe re n ces DeLany J 1999 Stop the cycle of chronic pain with neuromuscular therapy's 6-point system. Massage Magazine 79:54-66 American College of Rheumatologists 1990 Criteria for the classifi­ cation of fibromyalgia. Arthritis and Rheumatism 33:160-172 Dexter J, Simons 0 1981 Local twitch response in human muscle evoked by palpa tion and needle penetration of a trigger point. Anderson R, Wise 0, Sawyer T et a1 2005 Integration of myofascial Archives of Physical Medicine and Rehabilitation 62:521-522 trigger point release and paradoxical relaxation training treat­ ment of chronic pelvic pain in men. Journal of Urology Digiesi V, Bartoli V, Dorigo B 1 975 Effect of proteinase inhibitor on 174(1): 155-160 intermittent claudication or on pain at rest in patients with peripheral arterial disease. Pain 1 :385-389 Awad E 1973 Interstitial myofibrositis. Archives of PhYSical Medicine 54:440-453 Elvin A, Siosteen A-K, Nilsson A et al 2006 Decreased muscle blood flow in fibromyalgia patients during standardised muscle exer­ Awad E 1990 Histopathological changes in fibrositis. In: Fricton J, cise: a contrast media enhanced colour doppler study. European Awad E (eds) Advances in pain research and therapy, vol 17. Journal of Pain 10(2):137-144 Raven Press, New York, p 248-258 Fishbain 0, Goldberg M, Meagher BR et al 1986 Male and female Baldry P 1993 Acupuncture, trigger points and musculoskeletal chronic pain patients categorized by DSM-III psychiatric diag­ pain. Churchill Livingstone, Edinburgh nostic criteria. Pain 26:181-197 Barrell J-p 1 996 Manual-thermal diagnosis. Eastland Press, Seattle Fricton J, Kroenig R, Haley 0 et al 1985 Myofascial pain syndrome Beal M 1 983 Palpatory testing of somatic dysfunction in patients of the head and neck: a review of clinical characteristics of 164 patients. Oral Surgery 6:615-663 with cardiovascular disease. Journal of the American Osteopathic Association 82(11):73-82 Fryer G, Hodgson L 2005 The effect of manual pressure release on Bengtsson A, Heruikkson K, Larsson J 1986 Reduced high energy myofascial trigger points in the upper trapezius muscle. Journal phosphate levels in the painful muscles of patients with primary of Bodywork and Movement Therapies 9(4):248-255 fibromyalgia. Arthritis and Rheumatism 29(7):817-821 Bennett R 1989 Physical fitness and muscle metabolism in the Granges G, Littlejohn G 1993 Prevalence of myofascial pain syn­ fibromyalgia syndrome: an overview. Journal of Rheumatology drome in fibromyalgia syndrome and regional pain syndrome. 16(SuppI 19):28-29 Journal of Musculoskeletal Pain 1 (2):19-34 Boyle W, Saine A 1988 Naturopathic hydrotherapy. Buckeye Naturopathic Press, East Palestine, OH Grieve G (ed) 1986 Modem manual therapy. Churchill Livingstone, Bradley 0 1 999 In: Gilbert C (ed) Breathing retraining advice from Edinburgh three therapists. Journal of Bodywork and Movement Therapies 3(3): 1 59-167 Gunn C 1980 Prespondylosis and some pain syndromes following Brewer B 1 979 Aging and the rotator cuff. American Journal of denervation supersensitivity. Spine 5(2):185-192 Sports Medicine 7:102-1 1 0 Burckhardt CS, Archenholtz B , Mannerkorpi K et a l 1 993 Quality of Gunn C 1 997 Radiculopathic pain: diagnosis and treatment of seg­ life of Swedish women with fibromyalgia syndrome, rheuma­ mental irritation or sensitization. Journal of Musculoskeletal toid arthritis or systemic lupus erythematosus. Journal of Pain 5(4):119-134 Musculoskeletal Pain 1:199-207 Cailliet R 1991 Shoulder pain. F A Davis, Philadelphia G unn C Milbrandt W 1 978 Early and subtle signs in low back Chaitow L 1996a Palpation skills. Churchill Livingstone, Edinburgh sprain. Spine 3:267-281 Chaitow L 1996b Modern neuromuscular techniques. Churchill Livingstone, Edinburgh Headley B J 1993 Muscle inhibition. PhYSical Therapy Forum 24 Chaitow L, DeLany J 2003 Neuromuscular techniques in orthope­ November:1 dics. Techniques in Orthopaedics 18(1):74-86 Charkoudian N 2003 Skin blood flow in adult human thermoregu­ Henriksson K 1999 Is fibromyalgia a distinct clinical entity? Pain lation: how it works, when it does not, and w hy. Mayo Clinic mechanisms in fibromyalgia syndrome. A myologist's view. Best Proceedings 78(5):603-61 2 Practice and Research Clinical Rheumatology 13:455-461 Chikly B 1996 Lymph drainage therapy study guide level 1 . VI Publishing, Palm Beach Gardens, FL Holzberg A S, Kellogg-Spadt S, Lukban J C et al 2000 The Chikly B 2001 Silent waves: theory and practice of lymph drainage evaluation of transvaginal Thiele massage as a therapeutic therapy with applications for lymphedema, chronic pain and intervention for women with Ie. Presented at The National inflammation. IHH Publishing, Scottsdale, A2 Institute of Diabetes and Digestive and Kidney Diseases, Chu J 1995 Dry needling (intramuscular stimulation) in myofascial Interstitial Cystitis and Bladder Research Symposium, October pain related to lumbosacral radiculopathy. European Journal of 19-20, 2000 Physical Medicine and Rehabilitation 5(4):106-121 Cohen J, Gibbons R 1998 Raymond Nimmo and the evolution of Holzberg A, Kellog-Spadt S, Lukban J et al 2001 Evaluation of trigger point therapy. Journal of Manipulation and PhYSiological Therapeu tics 21(3):167-172 transvaginal Theile massage as a therapeutic intervention for women with interstitial cystitis. Urology 57(6 SuppI 1):120 Hong C 1996 Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Archives of Physical Medicine and Rehabilitation 77(11):1161-1166 Hong C-Z 2000 Myofascial trigger points: pathophysiology and cor­ relation with acupuncture points. 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6 Trigger points 1 23 Hong C-Z, Simons 0 1992 Remote inactivation of myofascial trigger Mense S 1993 Peripheral mechanisms of muscle nociception points by injection of trigger points in another muscle. and local mu'scle pain. Journal of Musculoskeletal Pain Scandinavian Journal of Rheumatology 94(Suppl):25 1 (1):133-170 Hong C-Z, Chen Y-C, Pon C, Yu J 1993 Immediate effects of various Mense S, Simons 0, Russell I J 2001 Muscle pain: understanding its physical medicine modalities on pain threshold of an active nature, diagnosis, and treatment. Lippincott Williams and myofascial trigger point. Journal of Musculoskeletal Pain Wilkins, Philadelphia 1 (2) :37-53 National Board of Chiropractic Economics 1993 Chiropractic treat­ Hou C-R, Tsai L-C, Cheng K-F, Chung K-C, Hong C-Z 2002 ment procedures, in job analysis of chiropractic (Table 9-11). Immediate effects of various physical therapeutic modalities on Greeley, CO cervical myofascial pain and trigger-point sensitivity. 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Journal of Applied Physiology Lewit K 1992 Manipulative therapy in rehabi lita tion of the locomo­ 99 :1977-1984 tor system. Butterworths, London Shealy C N 1984 Total life stress and symptomatology. Journal of Lowe W W 1995 Orthopedic and sports massage reviews. Holistic Medicine 6(2): 112-129 Orthopedic Massage Education and Research Institute, Bend, Simons 0 1987 Myofascial pain due to trigger pOints. Monograph 1, OR International Rehabilitation Medicine Association, Houston, TX Lukban L Whitmore K, Kell og-Spadt S et al 2001 The effect of man­ Simons 0 1988 Myofascial pain syndromes: where are we? Where ual physical therapy in patients diagnosed with interstitial cysti­ are we going? Archives of PhYSical Medicine and Rehabilitation tis, high-tone pelvic floor dysfunction, and sacroiliac 69:207-211 dysfunction. Urology 57(6 SuppI 1):121-122 Simons 0 1989 Myofascial pain syndromes. Current therapy of McCain G, Bell 0, Mai F et al 1988 A controlled study of the effects pain. 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1 24 CLI N I CAL APPLICATI O N O F N E U R O M U SC U LA R TECH N IQ U E S : T H E U PPER B O DY Simons 0, Travel l J, Simons L 1999 Myofascial pain and dysfunc­ Van Why R 1994 FMS and massage therapy. Privately published Ward R (ed) 1997 Founda tions of osteopathic medicine. Williams tion: the trigger point manual, vol 1 : upper half of body, 2nd edn. Williams and Wilkins, Baltimore and Wilkins, Baltimore Simons 0, Hong C-Z, Simons L 2002 Endplate potentials are com­ Weiss J M 2001 Pelvic floor myofascial trigger points: manual ther­ mon to midfiber myofascial trigger points. American Journal of Physical Medicine and Rehabilitation 81 (3) :212-222 apy for interstitial cystitis and the urgency-frequency syndrome. Sola A E, Rodenberger M L, Gettys B B 1951 Incidence of hypersen­ Journal of Urology 166:2226-2231 sitive areas in posterior shoulder muscles. American Journal of Wiederhol t W C 1970 'End-plate noise' in electromyography. Physical Medicine 34:585-590 Neurology 20:214-224 Straus S 1991 History of chronic fatigue syndrome. Review of Wittlinger H, Wittlinger G 1982 Tex tbook of Dr Vodder's manual Infectious Diseases 13:S2-S7 lymph drainage, vol l : basic course, 3rd edn. Karl F Haug, Swerdlow B, Dieter N 1992 Evaluation of thermography. Pain Heidelberg 48:205-213 Wolfe F, Simons 0 C, Fricton J et a l 1 992 The fibromyalgia and TravelI J, Simons 0 1 983a Myofascial pain and dysfunction: the trig­ myofascial pain syndromes: a preliminary study of tender points ger point manual, vol l : upper half of body. Williams and and trigger points in persons w i th fibromyalgia, myofascial pain Wilkins, Bal timore syndrome and no disease. Journal of Rhewnatology Travell J, Simons 0 1983b Low back pain (Pt 2). Postgraduate 19(6) :944-951 Medicine 73(2):81-92 Yunus M 1993 Research in fibromyalgia and myofascial pain syn­ Travel! J, Simons 0 1992 Myofascial pain and dysfunction, vol 2 . dromes. Journal of Musculoskeletal Pain 1 ( 1):23-41 Williams and Wilkins, Bal timore Zink J 1981 The posterior axillary folds: a gateway for osteopathlc Tullos H, Bermet J 1984 The shoulder in sports. I.n: Scott W (ed) treatment of the upper extremities. Osteopa thic Annals Principles of sports medicine. Williams and Wilkins, Baltimore 9 ( 3 ) : 8 1-88

1 25 Chapter 7 The internal environment This chapter focuses on the body's self-regulatory processes CHAPTER CONTENTS and systems that are involved in metabolism, repair and Local myofascial inflammatory influences 125 healing, with particular focus on the role these play in the Pain progression 126 Sensitization 126 p�r-oddeupcthtioenxpolfopraaitnio. nThoef scope of this text does not allow for Mecha nisms of ch ronic pain 126 diseases of the endocrine or diges­ Glutamate: a contrary view of the cause of tIVe systems, nor the numerous visceral pathologies that the tendon pain 127 patient might face. However, it is important that the practi­ Acute (lag) phase of the infla m m atory response 128 Regeneration (repair) phase 128 tioner is mindful of the ways these systems and processes, Remodeling phase 128 �aseinwgeollf as neurotoxic substances, affect the state of well­ Difference between degenerative a n d inflam matory the patient. Although the influences they are making processes 129 m the patient's wellness profile may not be as obvious as Antiinfla m matory nutrients and herbs 129 What about antiinfla m matory medication? 130 that of posture or range of motion, their impact on the body Controlled scarring - friction a n d prolothera py 130 When inflammation becomes global 131 and on health can be just as substantial as the external Hormonal influences 131 Muscles, joints and pain 140 (close) environment (see Volume 2, Chapter 4). Reflex effects of m uscula r pain 141 Source of pain 142 In a normal body with normal stressors, systems are Is it reflex or local? 142 Radicular pain 142 designed to maintain control of the levels of hydration, Are the reflexes normal? What is the source degree of metabolism, proliferation of repair materials of the pain? 142 and so forth. Most of the time this goes unnoticed by the Differentiating between soft tissue and joint pain 143 Neuropathic pain 143 person; however, occasionally 'something happens' that Neurotoxic elements and neuropathic pain 144 Effects of pH cha nges th rough breathing 149 causes 'normal' to become abnormal. Thermal, circula­ Alkalosis and the Bohr effect 149 Deconditioning a n d unbalanced breathing 149 tory, hormonal or any number of other processes become Caffeine in its various forms 150 When should pain and dysfunction be left alone? 1 51 altered, with a proliferation of bizarre symptoms and Somatization 152 How is one to know? 152 consequences. Pain management 1 54 Gunn's view 154 As practitioners, we are faced with the apparent paradox of Questions 154 Pain control 154 recognizing the importance, for instance, of inflammation in healing and of pain as an alarm signal, and yet are confronted with patients who demand the removal of these undesirable (to them) processes. Addressing this situation calls for an abil­ ity to explain and educate the patient as to the 'meaning' of symptoms as well as having the understanding and skill to omftoed�uplaiate?tTh�esfeu, rwthitehrouuntdseurpsptarnedssitnhgis the important roles they concept, let us begin by consJdermg mflammation and its role in healing. lOCAL MYOFASCIAllNFlAMMATORY INflUENCES In response to trauma and other abuses, defensive repair processes commence within myofascial structures with a

1 2 6 CL I N I CA L A PPL I CAT I O N O F N E U R O M U S CULAR T E C H N I Q U E S: T H E UPPER B O DY primary focus on reorganization and repair of damaged tis­ chronic pain what are known as wind-up type mechanisms sues. The coordinated achievement of these processes, and long-term potentiation (LTP) play roles in neuroplastic­ influenced by a plethora of biochemical mediators, occurs ity to cause hyperalgesia and allodynia. Wind-up is a pro­ under the general heading of 'inflammation' although, as gressive increase in the magnitude of the C-fiber evoked will become clear in this chapter, not all the processes under response. This may also produce some characteristics of that heading involve actual inflammation. Inflammation central sensitization, including expansion of the receptive that is not confined to myofascial tissues is discussed later fields and enhanced responses to C-fiber stimulation (Li in this chapter. et aI1999). These homeostatic adaptations usually take place in an Abnormal processing allows transmission of signals orderly mcumer, although the stages involved can vary along the central nervous system pathways, independent of quite considerably in temporal terms, depending on the sta­ the degree of nociception that is occurring in the periphery. tus of the individual and associated conditions (hygiene, for The term central sensitization refers to an increase in spinal example). There are three stages of inflammation (Toumi & cord neuronal excitability and a decrease in threshold. In Best 2003), commonly referred to as the acute response (lag) simple terms, the perceived pain may be greater than the phase, the regeneration phase and finally, if all is going well, injury would seem to warrant, due to increased sensitivity the remodeling phase (Liebenson 2006). of the nervous system itself, or of the part of the brain regis­ tering the pain messages - virtually as though the 'volume' The healing process needs to involve capillary repair and has been turned inappropriately high. new growth, proliferation of fibroblasts, deposition of colla­ gen and scar tissue formation. It is always worth reminding MECHANISMS OF CHRONIC PAIN ourselves that these types of inflammatory process are usu­ ally beneficial and have a great healing potential. Chronic pain is characterized by an abnormal sensitivity that may be due to generation of pain in response to low­ PAIN PROGRESSION threshold mechanoreceptive A-fibers that normally gener­ ate innocuous sensations (Woolf & DoubeI1994). For the individual to become aware of pain, peripheral noci­ ceptors (afferent neurons that respond to noxious stimuli) A decrease in non-nociceptive input may lead to pain by need to be activated (Davis 2001). These then stimulate neu­ a deafferentation mechanism, sometimes described as rons in the spinal cord (Carr & Goudas 1999). At the cord 'burning, raw, or searing' or as a 'tingling, numb sensation' level, pain signals may be both transmitted to the brain, as (Tasker & Dostrovsky 1989). well as being modified. Specific areas of the brain, such as the thalamus and brainstern, receive the nociceptive infor­ Changes in spinal sensory processing may occur without mation and have the ability to initiate descending inhibition. changes in blood flow (Andrews et a11999) or actual inflam­ mation (Alfredson et al 1999) (see details of this in discus­ Following joint or muscle injury, the spinal cord processes sion of tendon pain below). Mediated by low-threshold painful information and influences inflammatory responses mechanosensitive afferents projecting to sensitized dorsal (Dickenson et al 1997). The chemicals that are released in horn neurons, the nociceptive processes are qualitatively response to injury include potassium (from damaged cells), altered in patients with chronic myofascial pain (Bendtsen serotonin (from platelets), bradykinin (from plasma), hista­ et al 1996). Patients suffering from chronic whiplash syn­ mine (from mast cells), prostaglandins (PGE2, from dam­ drome (Johansen et a11999) and patients with fibromyalgia aged cells), leukotrienes (from damaged cells) and substance (Sorensen et al 1998) have a generalized central hyperex­ P (SF, from primary afferent fibers) (Purves et aI1996). citability of the nervous system, representative of central sensitization. Inflammation increases the sensitivity of the neural recep­ tors, both in the periphery and in the central nervous sys­ There is ample evidence that indicates diim nished tem, by altering the membrane properties of nociceptors, endogenous opioid (i.e. self-generated pain modulating) sys­ permitting a higher discharge frequency, and contributing to tems with chronic pain (Bruehl et al 1999). The functional hyperalgesia by activating synapses that are usually inactive result is hyperalgesia and spontaneous pain associated with (Djouhri & Lawson 1999, Li & Zhou 1998). Inflammatory tissue injury. Pain can also be biochemical in origin, even in pain and the sensitization of peripheral nociceptors can be apparently normal structures. Chemical mediators involved very rapid and may involve non-neuronal cells such as mast in nociceptive processing include neuropeptides, such as cells, neutrophils, fibroblasts, and macrophages (Mendell dynorphin, substance P and calcitonin gene-related peptide, et al 1999, Mense et aI2001). and excitatory amino acids, such as NMDA (N-methyl­ D-aspartic acid that mimics glutamate) (Dubner & Ruda 1992, SENSITIZATION Khan et aI2000). Patients suffering from chronic whiplash syn­ drome, for example, may have a generalized central hyperex­ Chronic pain can be due to tissue injury, nervous system citability from a loss of tonic inhibitory input (disinhibition) injury, or both (Woolf et al 1998). In the development of and/or an increase in excitatory input (partially chemically induced) contributing to dorsal horn hyperexcitability. This

7 The internal environment 1 2 7 may lead to dysfunction of the motor system. The aim of discussion, which the authors of this text find unfortunate, treatment should be not only to relieve pain but also to since its application in the acute stage would be most allow for proper proprioception (Parkhurst & Burnett 1994). appropriate as an inflammatory mediator. A fascinating link between emotion, endogenous chemical The risks of the use of antiinflammatory medication, and pain modulation and levels of chronic pain experienced has alternatives, are discussed later in this chapter. As will be been identified. For example, individuals chronically defi­ seen in Chapter 13, a variety of neuromuscular approaches, cient in endogenous opioid activity appear to have less abil­ including attention to the activities of active myofascial trig­ ity to inhibit emotions and physiological arousal, resulting in ger points and to manual release of increased muscular ten­ a strong and overtly expressive style of anger management. sion, offer alternative and complementary choices. This suggests that chronically low levels of opioid activity may be a common factor underlying development of both GLUTAMATE: A CONTRARY VIEW OF THE CAUSE the way anger is expressed (i.e. violently) and elevated pain sensitivity (Bruehl et a12002, Gregg & Siegel 2001). OF TENDON PAIN An elbow example But what if 'epicondylitis' - as described by Hume et al (2006) above - is inaccurate and the painful problem does not A standard medical view of the adaptive sequence, and the involve an inflammatory process after all? correct terminology associated with painful and inflamed joint tissues as they move from acute to chronic dysfunc­ Surprisingly, it appears that the actual causes of chronic tion, are encapsulated in the description of elbow injuries tendon pain remain unknown, and even though tendon by Hume et al (2006). They remind us that the incidence of biopsies commonly show no inflammatory activity, anti­ epicondylar injuries in those sports associated with over­ inflammatory medications are nevertheless commonly head or repetitive arm actions (baseball, for instance) are used. Wilson & Best (2005) note that: frequent and often severe. Histologic descriptions oftendinopathies have demonstrated • Acute elbow injury that results in inflammation should disordered collagen arrangement together with increased be termed epicondylitis, commonly the result of valgus proteoglycan ground substance and neovascularization. It is forces with medial distraction and lateral compression. unclear if these chronic degenerative changes are preceded consistently by an acute inflammatory response; therefore, • The more chronic stage of epicondylosis develops over a the designation of tendon pain as 'tendonitis' may be a mis­ longer period of time due to repetitive forces leading to nomer. The terms 'tendinopathy' and '[tendinosisl' are more structural changes in either epicondylar tendon. What the appropriate and should be used to describe these clinical enti­ patient feels, epicondylalgia, refers to elbow pain at either ties in the absence ofbiopsy-proven histopathologic evidence the medial or lateral epicondyle relating to tendinopathy ofacute inflammation, particularly in patients who have had of the common flexor or extensor tendon origins at these symptomsfor more than afew weeks. points. In other words, the suffix use of -itis or -osis is dependent Pain in such settings is usually associated with gripping, upon the stage of inflammation, acute versus chronic, resisted wrist extension and certain movements, such as in respectively. tennis and golf, hence the common terms 'tennis elbow' (lat­ eral epicondylitis) and 'golfer's elbow' (medial epicondylitis). A process of intratendinous microdialysis was employed by Scandinavian researchers (Alfredson 2005) to investigate Standard medical attention of corticosteroids and elbow human tendons. They found normal prostaglandin E2 (PGE2) straps may be used for treatment; however, as Hume et al levels and no proinflammatory cytokines, in people with make clear, there is 'very limited prospective clinical or exper­ chronic painful tendinosis (Achilles' and patellar). These imental evidence for their effectiveness'. Therefore, Hume findings show that there is no PGErmediated intratendi­ et al assert that, 'the most effective modalities of treatment nous inflammation, at least in the chronic stage of these are probably rest (the absence of painful activity) combined conditions. with cryotherapy in the acute stage', followed by anti­ inflammatory medication, heat (ultrasound) and cortisone However, the neurotransmitter glutamate (a potent mod­ injections, as well as rehabilitation exercises. W hile the ulator of pain in the central nervous system and its most authors of this text agree that this approach would allow the profuse excitatory neurotransmitter) has been found in natural transition from the acute to the regeneration and abundance in painful human tendons (Alfredson et al 2001, remodeling phases of recovery, it is suggested that cortisone Alfredson 2005). Microdialysis of these tissues has shown injections be considered only when all other measures have significantly higher glutamate levels in chronic painful failed and only if treatment of trigger points, joint mobility tendinosis (Achilles' and patellar), compared with pain­ and habits of use have been thoroughly addressed. free normal control tendons. Although the importance of Lymphatic drainage was apparently not considered in this these findings is not yet clear, they do suggest that anti­ inflammatory strategies may frequently be less than useful in such conditions.

1 2 8 C L I N ICAL A P P LICAT I O N OF N E U R O M U S CULAR TEC H N I QUES: T H E U P PER B O DY Central In the earliest stages, highly unstable fibrin structures process are laid down to secure the damaged tissues (Barlow & Willoughby 1992) and anything that stresses these further Peripheral (pressure, stretching, etc.) would, in all probability, aggra­ process vate and delay the healing process (Wah11989). Treatment (of B-afferent in the early stages - which can last up to a week - should fibers) ---/ therefore involve standard rest, ice, compression (bandaging or taping, for example) and elevation (RICE), with minimal stress to the tissues being allowed and certainly no active treatment. During the early stages following tissue injury, tensile strength is reduced and, therapeutically speaking, a primary task is to encourage the adaptive healing process by methods that promote early return of adequate tensile strength. Lymphatic drainage can be used in the acute phase and, as needed, throughout the entire inflammatory cycle. Figure 7.1 Schematic representation of neurogenic inflammation REGENERATION (REPAIR) PHASE cascade. Bk, bradykinin; PG, prostaglandins; SP, substance P, WBC, Under the influence of biological mediators such as IL-l, white blood cell. collagen synthesis occurs and new collagen fibers are laid down. Hunter (1998) suggests that this is a key time for ini­ Recent research into novel non-surgical methods of treat­ tiating constructive treatment: 'The tendency for the forma­ ment of tendinosis has shown promising clinical results. For tion of randomly oriented collagen fibers that restore example: structure but not flllction can be reduced by careful ten­ sioning of the healing tissue during the regeneration phase.' • painful eccentric calf-muscle training has been demon­ The key objective during this stage is the encouragement of strated to give good clinical short- and mid-term results enhanced tensile strength and stability, involving improved on patients with chronic painful mid-portion Achilles functional alignment of collagen fibers. tendinosis (Fahlstrom et a12003, Mafi et a12001) Liebenson (2006, p. 15) agrees: • good clinical results were associated with decreased ten­ don thickness and a structurally more normal tendon Some form of local tissue immobilization is usually advis­ with no remaining pain-inducing neovessels (Alfredson able during the [acute} inflammatory phase, which usually et a12003) peaks at approximately the third day after injury. Toward the end of the [acute] inflammatory phase, fibroblasts are • a specially designed treatment, using ultrasound-guided found in increasing numbers in the injured area. These injections of the sclerosing agent polidocanol, targeting the fibroblasts contribute to scarformation .. . connective tissue neovessels outside the tendon, has been shown to cure scarformation will persist and becomefibrotic, rather than tendon pain in pilot studies in a majority of the patients be absorbed, if the acute inflammatory reaction is allowed to (Ohberg & Alfredson 2003). persist. . . . During the repair phase, passive and active motion of the tissues positively affects the injured tissues. ACUTE (LAG) PHASE OF THE INFLAMMATORY RES POI\\ISE REMODELING PHASE The initial acute inflammation response results from tissue As collagen crosslinkage increases, stability returns but often injury, which can be on a microscopic cellular level or could at the expense of mobility. An understanding of the proper­ involve gross damage. This stage is characterized by initial ties of connective tissue and fascia allows for the selection vasodilation, increased local vascular permeability, tender­ of appropriate treatment strategies (see notes on fascia in ness, heat and edema. The way the organism reacts to trauma Chapter 1). Slow deliberate movements that localize tension involves both local and systemic (neuroendocrine) responses. to the injury site, as precisely as possible, are considered Numerous chemical mediators are involved in these useful early at this stage. In order to prevent undue loss of processes, including bradykinin, prostaglandins, leukotrienes, pliability during this phase, treatment that carefully encour­ cytokines, oxygen metabolites and enzymes (Fig. 7.1). ages full range of movement is helpful. Eventually, func­ tional movements, such as those encountered in daily life, During this phase the early repair of injured tissues com­ are encouraged. Pain-avoidance behaviors should be recog­ mences, with damaged or dead cells being replaced. nized and attempts made to reassure the patient to continue Various cytokines are thought to be intimately involved at this early inflammatory stage, primarily interleukin 1 (IL-1).

7 The internal environment 1 2 9 Injury cycle which are, in fact, degenerative. In such conditions there may be scant evidence of the beneficial influences of inflammation. Joints and ligaments TIlis 'mistaken identity' may occur, he notes, in Achilles ten­ Effusion dinitis and patella tendinitis, a view that is evidence based (Kannus 1997). Deconditioned Appropriate care Neglect or adverse Positive treatment 'Evidence . . . suggests that degenera tive tendon changes outcomes outcomes are evident in one third of the healthy urban population aged 35 or more.' Hunter (1998) reports that, at biopsy, degenera­ Excessive scarring Minimal scarring tive changes (e.g. calcifying tendinopathy) may be found Regeneration and that, without inflammation, there will be no stimulus to Intraarticular adhesions Repair healing. No pain Extraarticular adhesions Full strength ANTIINFLAMMATORY NUTRIENTS AND HERBS Continued pain Loss of function Full range If inflamma Loss of range modifies it is likely to reduce the level of perceived pain. It is Loss of power (atrophy) Hypertrophy important to keep in mind that although inflammation is Tendency to reinjure Normal movement patterns unpleasant it is a vitally important process in repairing (or Negative psychological effects defending against) damage, irritation or infection. Therefore No psychological residue antiinflammatory strategies (use of cryotherapy, medication, nutritional approaches, etc.) need to aim at a limited degree of 7.2Figure Schem atic representation of the injury cycle. reduction, rather than total elimination of this process, during the acute phase following tissue inj ury. movement therapies even in the face of some types of dis­ comfor t. As noted in this chapter, a major fea ture of localized inflammation involves prostaglandins and leukotrienes Liebenson (2006, p. 21) explains this shift in clinical (Djupsjobacka et aI1994). These are largely dependent upon thinking: the presence of arachidonic acid, which the body manufac­ tures mainly from a nimal fats. Reducing animal fat (meat, A paradigm shift from a traditional biomedical model to a poultry, dairy) intake cuts down levels of the enzymes tha t biopsychosocial one has taken firm hold in a spinefield. The help produce arachidonic acid (Donowitz 1985). biopsychosocia/ approach teaches us that the old adage 'let pain be your guide' can actually reinforce illness behavior Cold-water fish oil, on the other hand, provides anti­ such asfear-avoidance behavior. The more modern report of inflammatory eicosapentenoic acid (EPA), which interacts findings reassures patients that they do not have a disease with the metabolites of arachidonic acid to soften i ts effects (tumor, infection, and fracture) and that staying active will in the inflammatory process (Terano et a l 1986) . Five to ten actually speed recovery. Learning that pain does not always 1 000 mg EPA capsules daily are commonly taken to main­ warn of impending harm or damage can empower patients tain a reduction - but not elimination - of vital inflamma­ to remain active to avoid disability, and prevent the transi­ tory processes (Moncada 1986). tionfrom acute to chronic pain. Antiinflammatory (proteolytic) enzymes, often derived DIFFERENCE BETWEEN DEGENERATIVE AND from plants, have a gentle but substantial antiinflammatory INFLAMMATORY PROCESSES influence. These include bromelaine, which comes from the pineapple stem (not the fruit), and papain from the papaya Hunter (1998), quoted above, makes a clear distinction plant. It is necessary to ensure around 2-3 g of one or the between many conditions previously labeled as inflanunatory other are taken (bromelaine seems to be more effective) spread through the day, away from meal times, as part of an antiinflammatory, pain-relieving strategy (Cichoke 1981, Taussig 1988, Walker et al 2002, Werbach 1991). These veg­ etable enzymes can be taken before events, such as a marathon, to reduce subsequent tissue damage. Seaman (2006) suggests that potassium and magnesium are significantly important nu trients, generally overlooked, and tha t each could provide substantial antiinflammatory benefits as well as valuable pH influences. Deficiencies of either are critical factors in the development of chronicinflam­ mation. Glucose u tilization is impaired and glycogen stores reduced when potassium is deficient, resulting in hypoxia, muscle weakness, cramps and pain. Magnesium (Mg) is

1 30 C L I N ICA L A P P L ICAT I O N OF N E UR O M U S CULAR T E C H N I Q U E S: T H E U P P ER B O DY necessary for ATP synthesis and mitochondrial fW1ction, and WHAT ABOUT ANTIINFLAMMATORY profoW1dly influences potassium homeostasis. Deficiencies in Mg may be associated with neurogenic inflammation, a MEDICATION? generalized nervous system hyperexcitability and height­ ened peripheral and central nociceptive activity (Seaman Steroidal (e.g. cortisone) and non-steroidal antiinflamam tory 2006). The importance of maintaining adequate levels of drugs (NSAIDs) are among the most widely used medica­ magneSium is supported by Jing et al (1995), who link low tions, prescribed and over the cOW1ter (OTC). Although there dietary and serum Mg to the development of cardiovascular may be a place for the use of these, based on clinical experi­ disease, atherosclerosis, hypertension and diabetes. With ence and the widely reported dangers of many of these drugs appropriate changes in diet, adequate intake of potaSSium (e.g. the COX-2 inhibitors such as rofecoxib (VIOXX), recalled may be acquired through foods such as fruits, vegetables in September 2004), the authors of this text are strongly of the and nuts. However, it is usually necessary to supplement opinion that other, potentially less harmful, methods should Mg since dietary sources alone may not resolve the issue be used in preference, whenever possible. (Seaman 2006). The words of researchers who are strongly in favor of the Barbagallo et al (2003) point to the intimate relationship use of antiinflammatory medication state the case for using of Mg to insulin, and insulin's modulating effects on the such drugs with caution. For example, Ehrlich (2004) states: shift of Mg into intracellular space. They also note: • Pain remains the leading reason for which patients con­ Intracellular Mg concentration has also been shown to be sult their doctors. effective in modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation­ • Pain also motivates over-the-counter sales of analgesic contraction coupling, and decrease smooth cell responsiveness medicines, to be taken orally or even transcutaneously. to depolarizing stimuli. A poor intracellular Mg concentra­ Prescription medicines usually follow attempts at self­ tion, as found in noninsulin-dependent diabetes mellitus medication that fail to achieve the desired results. (NIDDM) and in hypertensive patients, may result in a defective tyrosine-kinase activity at the insulin receptor • Acute pain usually subsides spontaneously but medi­ level and exaggerated intracellular calcium concentration. cines are needed W1til that occurs; in arthritic conditions­ Both events are responsible for the impairment in insulin especially osteoarthritis - antiinflammatory drugs work action and a worsening of insulin resistance in noninsulin­ best in short-term administration for flares that aggravate dependent diabetic and hypertensive patients. .. . [It] may chronic but tolerable pain. play a key role in modulating insulin-mediated glucose uptake and vascular tone. Wefurther suggest that a reduced • In cases of chronic pain that exceeds the level of easy tol­ intracellular Mg concentration might be the missing link erance, antiinflammatory drugs can reduce the pain to helping to explain the epidemiological association between tolerable levels more effectively than simple analgesics NIDDM and hypertension. and narcotic combinations. As to diet and inflammation, Seaman (2006) suggests: • The non-steroidal antiinflammatory drugs (NSAIDs) are among the most useful medicines providing an array of A diet that is pro-inflammatory will increase the inflamm.a­ drugs that differ chiefly in time of onset of action, dura­ tory potential ofcells and tissues, and the outcome is likely to tion of action and persistence in the blood. be the phenotypic expression ofa disease or syndrome related to inflammation such as pain, arthritis, cancer, heart disease, • The benefit they provide is pain amelioration; none is diabetes, Alzheimer disease, and most other chronic degener­ ative diseases ... we can craft a diet that is rich infoods that curative. are known to be anti-inflammatory . . . such a diet would be free of simple carbohydrates because they drive hyperinsu­ • The risks are well known and do not differ greatly linemia and the expression ofsyndrome X . .. Calories would be restricted to inhibit an increase infat stores which serve as among the drugs; unwanted gastrointestinal (GI) effects a depot of inflammation and a promoter ofsyndrome X. are the most common, but the skin, kidneys, liver and He concludes that dietary focus would be similar to the hW1ter-gatherer diet, Mediterranean-like diet and the poly­ blood forming organs may also be affected. [emphasis meal, suggesting that food choices would include fish, grass­ added] fed lean meats, omega-3 eggs, fruits, vegetables, nuts, olive oil and minimal grains, coupled with eating less and exercising CONTROLLED SCARRING - FRICTION AND more. Dietary and lifestyle changes, such as those discussed by Richard & Richards (2003) offer a similar approach (see PROLOTHERA PY hormonal discussion later in the chapter). Treatment that deliberately mildly inflames the structure may, in such cases, be seen to offer a therapeutic stimulus. Controlled friction carefully applied to such structures could induce a mild inflammatory response and assist in achieving this. Methods such as crossfiber friction, as advo­ cated by Cyriax (1962), could be selectively useful in such settings. In the case of the induction of a deliberate inflam­ matory response, antiinflammatory measures, such as those discussed above, should be delayed until desired outcomes have been achieved.