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    9

    Regional myofascial pain: diagnosis

    and management

    Mike Cummings*

    Medical Director

    5 Lime Terrace, London W7 3HE, UK

    Peter BaldryEmeritus Physician

    Millstream House, Old Rectory Green, Fladbury, Pershore, Worstershire WR10 2QX, UK

    This chapter defines and describes the condition that is known by the term myofascial triggerpoint pain syndrome. An outline is given of the current state of knowledge of the pathophysi-ology of myofascial trigger points, including the latest details from needle microdialysis in

    near real-time. The clinical features of this pain syndrome are summarised in general termsand the reliability of the clinical diagnosis is discussed.

    The clinical evidence for and against the common therapeutic interventions used in themanagement of myofascial pain is reviewed in detail and some tentative conclusions are reachedwith respect to needling therapies.

    Key words: myofascial pain; myofascial trigger point; needling therapy; physical therapy.

    INTRODUCTION

    Definitions

    The term regional myofascial pain is used clinically in at least two distinct ways. First it isused synonymously with the terms myofascial pain syndrome and myofascial triggerpoint pain syndrome to describe the specific clinical manifestation of a rather ubiquitousform of muscle pain that is derived from myofascial trigger points and which can be as-sociated with a number of other sensory, motor and autonomic phenomena. Secondly,

    * Corresponding author. Tel.: 44 2085799607.

    E-mail address: [email protected] (M. Cummings).

    1521-6942/$ - see front matter 2006 Elsevier Ltd. All rights reserved.

    Best Practice & Research Clinical RheumatologyVol. 21, No. 2, pp. 367e387, 2007

    doi:10.1016/j.berh.2006.12.006

    available online at http://www.sciencedirect.com

    mailto:[email protected]://www.sciencedirect.com/http://www.sciencedirect.com/mailto:[email protected]
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    the term regional myofascial pain is used by clinicians to refer to soft tissue pain in gen-eral, particularly in circumstances where a more specific diagnostic category, such astendinopathy or enthesopathy, is not apparent. This chapter is concerned with themore specific use of the term, i.e. with the myofascial trigger point pain syndrome.

    MYOFASCIAL TRIGGER POINT PAIN SYNDROME

    Former misconceptions concerning the cause of this syndromes pain

    The cause for pain developing in the muscles of a seemingly otherwise fit person forcenturies remained an enigma and, as a consequence of this there was for long no gen-eral agreement as to what to call the underlying disorder.

    Guillaume de Baillou (1538e1616), when Dean of the medical faculty at the Univer-sity of Paris, introduced the term muscular rheumatism for it. At the beginning of the19th century two British physicians Balfour1 and Scudamore2 expressed the opinion

    that the pain arises as a result of inflammation developing in the fibrous connectivetissue in skeletal muscle. A view that continued to prevail in Britain throughout thatcentury and one that was to lead Sir William Gowers, in 1904, during the course ofa lecture, given at what was then called the National Hospital for the Paralysed andEpileptic, London, to conclude that as muscular rheumatism develops as a result ofinflammation of the fibrous tissue in muscle we may conveniently follow the analogyof cellulitis and term it fibrositis.3 This name was then widely employed for someyears but once it became evident that there were no convincing histological changesto support the hypothesis the term was eventually abandoned and replaced by thenon-committal one of myalgia.

    The evolution of present day concepts

    It was the French physician Francois Valleix who, in 18414, was the first to observethat the pain in this disorder emanates from well defined focal points of tendernessand which were thus called by him les points douloureux.

    The next to support this view was the German physician Cornelius who, in 19035,called them nervenpunkte and went so far as to conclude that the nerve endings atthese sites are in a state of hyperactivity because of the effect on them of such factorsas altered weather conditions, physical exertion and emotional upsets.

    It may, therefore, be seen that by the beginning of the 20th century some of themore enlightened physicians had come to appreciate that what hitherto had beenvariously called either muscular rheumatism or fibrositis occurs as a result of thedevelopment of increased activity in nerve endings at specific points of tenderness.A view endorsed by Sir William Osler who, in the 1909 edition of his textbook ThePrinciples and Practice of Medicine6, when discussing the disorder, stated it is by nomeans certain that the muscular tissues are the seat of the disease. Many writers claim,perhaps correctly, that it is a neuralgia of the sensory nerves of the muscles.

    It was not, however, until the 1930s that objective clinical support for this viewbegan to appear. One of the first clinicians to provide this was Hunter, a physician

    in Canada who, in 1933, described cases in which abdominal pain emanated frompoints of tenderness in anterior abdominal wall muscles.7

    Then in 1936, Edeiken & Wolferth, physicians at the University of PennsylvaniaMedical School, reported that among patients with coronary thrombosis under their

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    care some had developed shoulder pain that could be reproduced by applying firmpressure to points of exquisite tenderness in muscles around the scapula.8

    The physician, however, who during the 1930s made the greatest contribution toour knowledge concerning the pathophysiology, diagnosis and treatment of what,currently, is called the myofascial trigger point pain syndrome was John Kellgren duringthe time he was working as a research assistant to Sir Thomas Lewis, the director of

    Clinical Research at University College Hospital, London.Lewis and Kellgren first carried out an experiment on healthy volunteer medical

    students. In this they injected pain-evoking hypertonic saline into muscles and ob-served that rather than the pain being experienced at the injection site it was feltsome distance away at what they called the zone of pain referral.

    Kellgren then turned his attention to patients with muscle pain.9 With respect tothese he said:

    A number of cases of fibrositis or myalgia have been investigated. Thedistribution of pain from normal muscles guided me to the muscles from which

    spontaneous pain may have arisen. Such muscles always presented tender spotson palpation and pressure on these spots reproduced the patients pain.

    He then went on to confirm that the pain arose as a result of nerve hyperactivity atthese tender points by showing that it could be alleviated, often for several days, byinjecting a local anaesthetic into the tissues at these tender sites.

    Janet Travells pivotal contributions to the subject

    During World War II, Kellgren served in the Royal Army Medical Corp. Following this

    he became Professor of Rheumatology at Manchester University, but his former studyof muscle pain was not renewed. Fortunately, however, during the 1940s, a youngAmerican physician, Janet Travell, decided to take up the study of the subject wherehe had left off. She did so having read how Kellgren had shown that widespread dullaching pain in muscle emanates from what an American orthopaedic surgeon had aptlycalled trigger points.

    Travells study of the subject led her to realise that pain in the disorder that hithertohad variously been called rheumatism, fibrositis, myalgia and a host of other synonymsarises not only from skeletal muscle itself but also from its fibrous connective tissue.She therefore, during the 1950s, in view of the Greek for muscle being myos, called the

    disorder the myofascial trigger point pain syndrome.Furthermore, she soon recognised that each muscle in the body has its own spe-cific pattern of myofascial trigger point pain referral and over the years, together withher colleague David Simons, published diagrams of these in two prestigiouspublications.10,11

    Prevalence of myofascial trigger points

    Myofascial trigger points (MTrPs) are recognised by many clinicians to be one of themost common causes of pain and dysfunction in the musculoskeletal system. They

    have been detected in the shoulder girdle musculature in nearly half of a group ofyoung, asymptomatic military personnel12 and with a similar prevalence in the masti-catory muscles of a group of unselected student nurses.13 Active MTrPs, those causingspontaneous pain, have been diagnosed as the primary source of pain in 74% of

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    96 patients with musculoskeletal pain seen by a neurologist in a community pain medicalcentre14 and in 85% of 283 consecutive admissions to a comprehensive pain centre.15

    Of 164 patients referred to a dental clinic for chronic head and nec k pain, 55% were

    found to have active myofascial trigger points as the cause of their pain16, as were 30% ofthose presenting with pain to a university primary care internal medicine group practicefrom a consecutive series of 172 patients.17 A study of musculoskeletal disorders in vil-lagers from rural Thailand has demonstrated myofascial pain as the primary diagnosis in36% of 431 subjects with pain during the previous 7 days.18

    Essential clinical features of MTrPs

    The essential clinical features of MTrPs are:

    A tender point within a taut band of skeletal muscle A characteristic pattern of referred pain (see Figures 1 and 2 for examples) Patient recognition of pain on sustained compression over the tender point

    Figure 1. These diagrams illustrate some of the more common myofascial trigger point sites (#) in the head

    and neck and their respective pain patterns.

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    A local twitch response (LTR) within the band of muscle on plucking palpationacross the fibres.

    Various classifications have been used for different presentations of MTrPs, but themost straightforward has been alluded to above. That is the distinction between activeand latent MTrPs. Active MTrPs are classified as those that cause spontaneous pain,while latent MTrPs have all the same clinical features without being responsible fora pain complaint.

    Pathophysiology of MTrPs

    The key pathophysiological abnormalities associated with MTrPs appear to be

    principally located at the centre of a muscle in its motor endplate zone. This zoneis where the motor nerve, on entering a muscle, divides into a number of brancheswith each of these having a terminal claw-like motor endplate embedded in the surfaceof a muscle fibre.

    Figure 2. These diagrams illustrate some of the more common myofascial trigger point sites (#) in the back

    and hip girdle and their respective pain patterns.

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    Each MTrP contains a neurovascular bundle. The principal contents of thisare motor nerve endings and group III and IV nociceptive sensory afferent nerveendings.19,20

    Sensory phenomena

    Tenderness has been investigated using pressure algometry and several studies havedemonstrated that this is a reliable tool for assessing MTrP sensitivity.21e23 Bendtsenet al investigated the nociceptive process in the MTrP pain component of 40 cases ofchronic tension-type headaches compared with 40 healthy controls.24 The relationshipbetween the pressure applied over an MTrP and the associated pain was found to belinear e that is increments in pressure were proportional to the resulting incrementsin pain. Over normal muscle the relationship was found to be non-linear; typicallyincrements in pressure over normal muscle do not cause pain until a threshold isreached, beyond which pain increases disproportionately. The authors therefore pos-tulated that myofascial pain is mediated by low-threshold mechanosensitive afferentsprojecting to sensitised dorsal horn neurons.

    Motor phenomena

    Whilst taut bands have been detected in muscle for a very long time25, the precisenature of the MTrP has remained elusive. It is only relatively recently that a pathophys-iological marker, in the form of spontaneous needle EMG activity, has been identifiedwithin a 1e2 mm nidus of a MTrP.26 Spikes (100e600 mV, biphasic, initially negative)and continuous low amplitude action potentials (10e80 mV) were recorded in thevicinity of an active MTrP, but only the continuous low amplitude action potentials

    could be recorded from latent MTrPs. There has been controversy over the likelysite of origin of this electrical activity. Hubbard & Berkoff postulated that the sourcewas intrafusal fibres within the muscle spindle26, but Hong & Simons have put forwarda strong argument in favour of dysfunctional motor endplates.27 It is unfortunate thatthis type of electrical activity is not specific to MTrPs and can be demonstrated in theendplate zone outside an MTrP, although it has not been demonstrated outside theendplate zone.28

    Spontaneous electrical activity (SEA) e referring to the continuous low amplitudeaction potentialse has been shown to vary significantly in amplitude between symptomaticpatients (suffering from tension headaches and fibromyalgia) and control subjects.26 In

    normal subjects with latent MTrPs, SEA recorded from the upper trapezius has beenshown to increase dramatically in amplitude as a result of psychological stress alone;29

    and phentolamine, an alpha adrenergic blocker, appears to diminish the amplitude andfrequency of spikes recorded from MTrPs in humans30 and in a rabbit model.31

    The local twitch response (LTR) has been studied electrophysiologically in bothman and the rabbit model.27 The muscle contraction of an LTR appears to occuronly within the taut band and the latency of the contraction following direct mechan-ical stimulation of the MTrP is consistent with a polysynaptic reflex. LTRs can beabolished by a local anaesthetic block, or by transection of the innervating nerve,and are diminished following cord transection, although they recover almost com-

    pletely after the period of spinal shock.27

    Couppe et al have contributed important work with MTrPs in the infraspinatusmuscle of humans.32 Nineteen young subjects with chronic shoulder and arm pain,who had an MTrP in the infraspinatus muscle, were examined. This point and

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    a non-tender control point in the same muscle were code-marked, in order to blindthe examiner. Around both points 20 concentric needle electromyographic (EMG)recordings were obtained at rest. More subjects had spontaneous EMG activity atthe MTrPs than at the control point. The EMG activity was interpreted as end-platenoise or spikes or both. The MTrP Root Mean Square amplitudes were significantlyhigher than at the control points. This is the first work to confirm the presence of

    SEA at MTrPs in a blinded study.Of the numerous other studies that have investigated SEA, it is important to mention

    Chen et al.33 This experimental study on the rabbit biceps femoris model demonstratesa reduction in amplitude of SEA at what is considered to be the equivalent of MTrPsfollowing therapeutic-style dry needling. This is soft evidence for the apparent immedi-ate benefit of needling in myofascial pain that is reported by clinicians in practice.

    Biopsy studies

    Simons28 suggests that highly contracted portions of muscle fibres, which he calls con-

    traction knots, may be a specific histological marker for the MTrP (Figure 3). Theywere first described in 1951 in biopsies of Muskelharten (muscle indurations)34

    and again in 1960 in biopsies from similar sites in patients described as having fibrosi-tis.35 In 1976 MTrP criteria were used to investigate canine muscle and sites that wereclinically equivalent to MTrPs in humans were examined histologically.36 Muscle cross-sections revealed some darkly staining, large, round fibres. The equivalent longitudinalappearance showed central bulges within some muscle fibres where there was a highlycontracted portion. Either side of this bulge the fibre was narrow and elongated to

    Figure 3. This is a diagrammatic representation of part of a myofascial trigger point showing two motor

    endplates (MEPs) and juxtapositional contraction knots (CKs); also a neurovascular bundle (NB) containing

    motor nerves (MNs), nociceptive and sensory afferents (SAs) and blood vessels (BVs) with closely associated

    sympathetic fibres. Note that in a normal muscle fibre (NMF) the sarcomeres are of equal length, but in

    a muscle fibre containing a contraction knot there is compensatory lengthening of sarcomeres on either side.

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    compensate for the central knot of contracted sarcomeres. More recently, these his-tological findings have been confirmed and further elaborated, with the use of electronmicroscopy, on biopsies of human gluteus medius MTrPs from fresh cadavers.37

    Since the demonstration of SEA from MTrPs, Simons has proposed that thecontraction knot is likely to be the source of this activity.38 He cites experimental re-search on mammalian skeletal muscle39 and the microscopic appearance of a contrac-

    tion knot in canine gracilis muscle36 to support his contention that the contractionknots observed in MTrP biopsies occur at the site of the motor endplate. He addsfurther support to this suggestion by observing that the longitudinal dimension ofthese knots is similar to the length of a motor endplate.

    In 2000, De Stefano et al performed a slightly different type of biopsy study ofMTrPs. They used immunohistochemistry to study substance P immunoreactive(SP-ir) nerve fibres in muscle biopsies from the upper trapezius of nine womenwith myofascial pain, nine women with fibromyalgia (FM) and nine healthy women.40

    They found no difference in numbers of SP-ir nerve fibres in the three groups ofwomen, but there were significant differences in the mean optical density of SP-ir

    nerve fibres, i.e. there were differences in terms of the quantity of substance P (SP)in the nerve fibres. SP may be taken as a marker for peripheral sensitisation, so it isinteresting to note that SP concentration was significantly greater in MTrP biopsiesfrom myofascial pain patients compared with FM patients, and SP concentration wassignificantly greater in biopsies from FM patients compared with healthy controls.

    Microdialysis

    Some rather innovative work was published by Shah et al in 2005.41 They used a fine,

    non-cutting needle (an acupuncture needle) as the basis for the development of a mi-crodialysis instrument to measure the in vivo biochemical milieu of muscle in near real-time at the sub-nanogram level of concentration. They used nine volunteers: threenormal, three with latent MTrPs in upper trapezius and three with active MTrPs inupper trapezius. Concentrations of protons, bradykinin, calcitonin gene-related pep-tide (CGRP), substance P (SP), tumour necrosis factor alpha, interleukin-1beta, sero-tonin and noradrenaline were found to be significantly higher in the active group thaneither of the other two groups (P< 0.01). pH was significantly lower in the activegroup than the other two groups (P< 0.03). After the needle was moved to obtainan LTR, a manoeuvre that is thought to be associated with therapeutic benefit, the

    concentrations of CGRP and SP in the active MTrP sites diminished significantly.This is rather preliminary work, in a small number of subjects, but it may be animportant step towards a fuller understanding of the elusive substrate of this appar-ently common muscle pain condition.

    Factors responsible for the development of MTrP activity

    Trauma

    The usual reason for MTrP nociceptive sensory afferent activity developing is the

    subjection of a muscle to the high intensity stimulation provided by trauma. Thismay be brought about either by a direct injury to the muscle or by the sudden orrepeated overloading of it. Alternatively, it may develop when the muscle is subjectedto repeated episodes of microtrauma such as occurs with a repetitive strain injury.

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    Anxiety

    MTrP activity may also be brought about when a patient of an anxious temperamentholds a group of muscles in a persistently contracted state.

    Muscle wasting

    MTrP activity is liable to develop when muscles have become weakened and wasted bymalignant disease or a neurological disorder. With respect to strokes, MTrP nocicep-tive pain is liable to develop when weakened muscles become overloaded duringattempts to restore movements to them during the recovery stage.

    Muscle ischaemia

    MTrP activity may arise when, because of arterial obstruction, the muscles of a limbbecome ischaemic.

    Visceral pain referral

    Pain arising as a result of visceral disease is frequently referred to both skin andmuscles. When this happens MTrPs in muscles situated in this zone of pain referralare liable to become active, with the production of superimposed MTrP pain.42

    Radiculopathic compression of motor nerves

    When pain occurs as a result of spinal nerve root compression, such as from spondy-losis or disc prolapse, pain may also arise as a result of the secondary development ofTrP activity in the paraspinal muscles.43

    Climatic causes

    MTrPs are liable to become active when the muscles containing them are exposed toadverse environmental conditions such as damp, draughts, excessive cold or extremeheat.44

    DIAGNOSIS OF MTrP PAIN SYNDROME

    Clinical manifestations

    Patient history

    Pain. This is by far the most common presenting complaint. Typically the pain isdescribed as deep, aching and poorly localised. It is usually restricted to one quadrantof the body, although complex patterns from multiple MTrPs may give a wider distribu-tion. It is important to determine the precise nature and pattern of the pain, as would bedone when taking a standard medical history. Paraesthesia is not uncommon in associa-tion with the pain and often confirms in the patients mind the false impression that theyhave a trapped nerve. Symptoms are generally exacerbated by activity; however, some

    light exercise involving gentle stretching of the affected muscle may relieve the aching.Some patients will find a tender point in muscle, particularly if the MTrP is in an

    accessible site; and a few will describe some sort of technique they have developedto relieve the pain, which usually involves the application of pressure to the MTrP.

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    Dysfunction. MTrP activity may lead to the development of various autonomic changes.These include lacrimation, regional pilomotor activity and excessive coldness of anextremity. MTrPs appear to affect proprioceptive function. In the cervical musculature,in particular sternomastoid, this may be responsible for dysequilibrium, even to theextent that the patient may describe true vertigo. In the limb musculature this mayresult in distorted weight perception. Motor dysfunction includes restricted range,

    weakness, reduced co-ordination and spasm in other muscles.

    Sleep. Myofascial pain may disturb sleep but, more importantly, sleep position oftenaggravates MTrP activity by allowing affected muscles to shorten.

    Age. MTrPs occur in all age groups but present most commonly in the middle years.The muscles of young active people are probably more resistant to injury, and fasterto repair, so less likely to develop or sustain active MTrPs. By comparison, the muscu-loskeletal system of the middle-aged adult is becoming increasingly degenerate, lessresilient and slower to heal. In general the middle-aged are less active, but engagein unaccustomed bouts of physical activity. They tend to suffer most with the painof active MTrPs. Latent MTrPs can be found in the majority of elderly people, causingstiffness and reduced active range of movement, but this age group present lessfrequently with the pain of active MTrPs.

    Sex. Women seem to present more frequently with myofascial pain than men. It hasnot been established whether myofascial pain is more common in women, or whetherthey are more likely to present with this type of pain. It is certainly true that pheno-typic differences can influence biomechanical loading and, for the same mass, womentend to have wider hips and narrower shoulders than men. Biological factors such asthese may be important, but socio-economic differences in terms of working environ-ments may also have an influence. For example, a higher proportion of the male work-force performs physically strenuous jobs and it has been noted that these individualssuffer less from myofascial pain than sedentary workers.

    Examination findings

    Tender point. This is the key feature of an MTrP, although it is clearly not exclusive toMTrPs. A tender point is usually a discrete area in the soma, which, when pressure isapplied to it, produces more pain than its immediate surroundings. In a clinical setting,

    pressure is usually applied with the fingertips onto the surface of the body. The pres-sure is transmitted through a range of soft tissues that are compressed between theexaminers fingertips and an unyielding surface beneath. The latter is often bone, butmay be a soft tissue layer under tension and, hopefully, is not the examination couch!There are a number of sites on the human body that appear to be tender because ofinconsistency in the unyielding surface beneath. Pressure applied to these areas is con-centrated over a small volume of soft tissue, rather than distributed more widely andevenly to the surroundings. Thus consistent extrinsic pressure, whether applied withfingertips or an algometer, generates greater pressure within the soft tissues at thesesites than is produced in their surroundings, giving a false impression of tenderness.

    Therefore, it is always worth comparing tenderness at the site of a suspected MTrP,with the same anatomical site on the asymptomatic side of the body. In the myofascialpain syndrome, active MTrPs are rarely symmetrical, as opposed to fibromyalgia, inwhich tender points are widespread and often symmetrical.

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    When trying to determine which tissue is tender, it can be useful to stretch themuscle layer whilst palpating, or to get the patient to perform an isometric contractionwhilst putting pressure over the tender point. Both of these techniques tend toincrease the relative pressure in the muscle layer and, therefore, have some discrim-inative value.

    Taut band. The taut band associated with an MTrP is palpated by drawing the fingertipsof the examining hand forward and back perpendicular to the fibres of the relevantmuscle. The muscle should be placed on a slight stretch and the skin and subcutaneoustissues are moved with the fingertips as the muscle fibres are palpated. Some super-ficial muscles can be palpated between finger and thumb in a pincer grip and thetaut band is felt as the fibres are allowed to slip between the palpating digits. The lattertechnique often requires the relevant muscle to be slackened off.

    Pain. As an active MTrP is palpated, the patient will often exclaim thats it, or givea similar verbal indication that they recognise the pain. The pain is usually sufficientto cause the patient to give an involuntary jerk, withdrawing slightly from the palpatingfingers. This is referred to as the Jump Sign. It is very import to ask the patient if it istheir usual pain that is generated by applying pressure to the MTrP and to ask them toindicate the pattern of pain produced. The pain referral patterns produced by MTrPs inskeletal muscle are frequently characteristic of the specific muscle and, with experience,the musculoskeletal specialist can determine the most likely muscles involved from thehistory alone, so that detailed examination can be targeted to the relevant areas.

    Local twitch response. When the palpating finger is snapped across the taut band of anactive MTrP, there is often a detectable contraction of it (Figure 4). This local twitchcan be visible if the muscle is superficial, or may be felt by the examiner. The LTR ismore frequently encountered when directly needling the MTrP.

    Other examination findings. MTrPs invariably cause shortening of the affected muscleand may cause a reduction in power without muscle atrophy. Muscle shorteningresults in a decreased range of movement (ROM) of the associated joint or joints.This can be a very helpful sign, but its usefulness is determined by how easy it is tomeasure the relevant ROM in a clinical setting. Assessment of power is generally

    Figure 4. This figure illustrates the examination of a muscle for trigger points by snapping palpation across

    the fibres to elicit a local twitch response. The image on the right shows a local twitch within the fibres of

    the sternal head of the sternocleidomastoid muscle.

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    not useful in determining the presence of MTrPs; however, the manoeuvre used to testpower, resisted muscle contraction, often causes pain if the muscle tested is harbour-ing an active MTrP, especially if the resistance is applied with the muscle in a shortenedposition.

    Reliability of clinical features

    There have been several studies testing the inter-observer reliability of the examintionfor MTrPs. Those using untrained examiners failed to demonstrate reliability.45,46

    A further study using trained examiners gave a marginal result.47 A more recent study,using experienced clinicians, demonstrated reliability in its second phase after theexaminers underwent a 3 hour period of training.48 The following clinical featurestested are placed in order of overall inter-rater reliability:

    (1) Pain recognition

    (2) Taut band(3) Tender point(4) Referred pain(5) LTR.

    In 2001, Sciotti et al took this work further by demonstrating that two trainedexaminers, blind to each others findings, can reliably localise latent MTrPs in uppertrapezius with a precision that essentially approaches the physical dimensions of theclinicians own fingertips.49

    Simons recommends that the minimum acceptable criteria for diagnosing a myofas-

    cial TrP are the combination of spot tenderness in a palpable band of skeletal muscleand subject recognition of the pain, but he admits that palpation of a taut band isconditional on the accessibility of the muscle.28

    MANAGEMENT OF MTrP PAIN SYNDROME

    Needling therapies

    Needling of MTrPs is one of the most common treatments for myofascial pain in globalterms. This is because of the use of acupuncture in the East. Acupuncture is also pop-ular in the West, but not on such a scale, and is sometimes referred to as dry needling.Wet needling, or injection therapy, is perhaps more commonly applied in the West,with a variety of injected substances being used, ranging from the relatively innocuousphysiological saline to the toxin derived from Clostridium botulinum.

    The evidence for needling in myofascial pain

    A systematic review published in 2001 of 23 randomised controlled trials (RCTs)conclusively shows, when treating myofascial pain with trigger point injection, thatthe nature of the injected substance makes no difference to the outcome and that

    there is no therapeutic benefit in wet over dry needling.50

    These conclusions weresupported by all the high quality trials in the review.51e59 The authors of the reviewconcluded: The hypothesis that needling therapies have specific efficacy in the treat-ment of myofascial pain is not supported by the research to date, but this review

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    suggests that any effect derived from these therapies is likely to be derived from theneedle, rather than from either, an injection of liquid in general, or any substance inparticular. All groups in the review in whom trigger points were directly needledshowed marked improvement in their symptoms; therefore further research isurgently needed to establish the specific effect of trigger point needling, with emphasison the use of an adequate control for the needle.

    Subsequent to this review, a number of relevant studies have been published60e71;however, they would not substantially alter the conclusions of the review. T here is,perhaps, a little more weight in favour of there being a specific effect of needling61,63,64,but this is far from definitive. It does seem quite clear now, however, that botulinumtoxin injection does not offer any advantage over saline or local anaesthetic.67,68,71

    Recently there has been some interest in the use of the 5-HT3 receptor antagonisttropisetron for injection into MTrPs,72 following the demonstration of its efficacywhen administered systemically in patients with fibromyalgia.73 It has yet to be testedin a RCT of myofascial pain, but it may turn out to be the first substance that providesmore benefit than injection or needling alone. It seems that one of its actions is to

    prevent SP release from sensory nerves, and, as has been mentioned above, SP mayhave a role in mediating peripheral sensitisation in MTrPs.

    The mechanism of needling in MTrP pain

    The mechanism of action of direct needling in the deactivation of trigger points is un-determined. Despite the fact that a causal relationship has not been establishedbetween direct needling of trigger points and improvement in symptoms, a discussionof the potential mechanisms involved may still be useful in developing future researchquestions. Simons comments on the results of two trials that compare direct dry and

    direct wet needling of trigger points17,74 and concludes that the critical therapeuticfactor in both techniques is mechanical disruption by the needle.28 The common factoris certainly needle insertion into the trigger point; however, Hong has demonstratedthe importance of stimulating a LTR in achieving an immediate effect,74 and, withSimons, cites evidence that the LTR is mediated by a segmental spinal reflex.27 Fineet al performed a rigorous experimental study, in which trigger points were subjectto direct wet needling, and clearly demonstrated that an opioid mechanism wasinvolved in trigger point pain relief.75 In view of this evidence, combined with theapparent clinical effectiveness of superficial dry needling (a technique that does notinvolve direct penetration of the MTrP),76 it seems possible that the needle can

    work through sensory stimulation as well as through mechanical disruption and thiswould be consistent with the mechanism of action of acupuncture analgesia.77

    Non-needling therapies

    There is a great variety of these non-invasive therapies. The most commonly applied inclinical practice are probably physical treatments. Whilst they are given many differenttitles, most involve the application of some form of mechanical pressure to the MTrPor stretch ofthe affected muscle, or both. Travell developed the technique of stretch

    and spray.10

    This involves the use of a vapocoolant spray applied in a defined patternjust prior to stretching the involved muscle. The sudden sensory stimulus of the sprayacts as a distraction and reduces the discomfort from stretching a muscle shortenedby an MTrP. Various other techniques have been described to enhance stretching.

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    Post-isometric relaxation78 and reciprocal inhibition28 involve voluntary muscle con-traction by the patient of the target muscle or its antagonists, respectively. Accessorytechniques, including phased respiration and eye movements, can also be used toaugment stretching. Pressure has been applied to TrPs in the form of ischaemic com-pression, shiatsu, acupressure, pressure release and many forms of massage. Simonsgives a comprehensive account of reported therapies applied to MTrPs in the second

    edition of The Trigger Point Manual.28

    Despite the prevalent use of physical therapies in the treatment of myofascial pain,surprisingly few of them have been subjected to controlled clinical trials. In five pa-tients with bilateral active MTrPs in trapezius, Jaeger & Reeves randomly selectedthe side for treatment with stretch and spray and demonstrated a significant reductionin MTrP sensitivity (pressure pain threshold measured with an algometer) comparedwith the untreated side.79 Pain scores decreased significantly but did not correlatewith MTrP sensitivity. Gam et al performed a randomised controlled trial comparingultrasound, massage and exercise with sham-ultrasound, massage and exercise witha no treatment control group in a population of patients with MTrPs of the neck

    and shoulders.80 Ultrasound was shown to be ineffective. Both active treatmentgroups improved significantly compared to the control, but the latter was inadequateto conclude that massage and exercise had a specific effect. Interestingly, a muchhigher intensity ultrasound treatment (referred to as high-power, pain-threshold, staticultrasound) has subsequently proved to be more effective than conventional ultra-sound, when targeted at MTrPs before stretching.81

    MTrPs have become a popular target for enthusiasts of low level laser therapy (LLLT).Several randomised controlled trials have been reported and positive results82e86 haveexceeded the negative.87 A systematic review published in 1992 concluded that lasertherapy appears to have a substantial specific therapeutic effect.88 However, a plausible

    mechanism is still lacking as there is no sensory stimulation perceived from active LLLTand the photon beam has very limited penetrance. Moreover, experimental work byLundeberg has demonstrated that this type of laser stimulus has no demonstrable effecton nerve tissue.89,90

    Transcutaneous electrical stimulation of various sorts have been tested on MTrPs.Graff-Radford et al tested four modes of transcutaneous electrical nerve stimulation(TENS) and a no-stimulation control on 60 patients with myofascial pain. High intensityTENS was effective in reducing myofascial pain but not MTrP sensitivity. In view of thisit is not surprising that in a trial 9 years later of sub-threshold TENS applied to patientswith myofascial pain and dysfunction of the masticatory system, the active intervention

    proved no better than the sham.91

    Electrical stimulation over MTrPs with a pocket-sized stimulator has been shown to increase pain threshold algometer readings overthe treated points compared with a no treatment control,92 but whether this wouldcorrelate to clinically significant symptom relief has not been established; furthermore,

    Jaeger & Reeves have indicated that there may be no correlation between pain reduc-tion and MTrP sensitivity.79 Hsueh et al compared electrical nerve stimulation (ENS),using a standard TENS machine set at 60 Hz, with electrical muscle stimulation (EMS)at 10 Hz.93 The latter, but not the former, was sufficient to induce muscle contraction.A third group received a sham control. Sixty patients were randomised to the threegroups. ENS proved more effective for pain relief, but EMS resulted in a greater

    improvement in range of movement.Treatments that have been shown to be ineffective include sphenopalatine ganglion

    block for myofascial pain of the head and neck,94,95 occlusal splints for myofascial painof the jaw muscles96 and oral sumatriptan for myofascial pain of the temporal

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    muscles.97 Low dose clonazepam proved superior to placebo in the treatment of my-ofascial pain related to temporomandibular joint dysfunction,98 but benzodiazepinesare not suitable for lengthy treatment because of the risk of dependence.

    More unusual treatments involve mud baths and magnetic fields. According toa randomised controlled trial by Pratsel et al, mud baths containing sulphur com-pounds reduce the sensitivity of MTrPs compared to those that do not contain sulphur

    compounds.99 Pain scores in post-polio patients reduced significantly resulting fromthe application of 300e500 Gauss magnetic devices to their pain trigger points, com-pared with the use of placebo devices.100 More recently a different form of magneticstimulation (peripheral repetitive magnetic stimulation e rMS) has shown benefitbeyond control in trapezius MTrPs.101

    Prognosis

    Despite the lack of convincing evidence of specific efficacy for any of the therapies

    regularly applied to MTrPs, the empirical experience of clinicians treating myofascialpain is very positive. Simple clinical audit suggests that the majority of people getbetter with dry needling,102 and the same probably applies to the popular non-needlingphysical therapies. As a general rule, myofascial pain syndromes which have been pres-ent for 6 months or less appear to be curable, but those which have been present forlonger, or have followed a chronic relapsing course, can only be treated symptomat-ically, with a latent tendency to relapse remaining (White A, pers comm., 1994).

    MTrPs may appear to move during treatment. This is likely to be an apparent move-ment rather than actual movement of a specific MTrP and can occur as a result oftreatment of a series of satellite MTrPs. If the key MTrP is identified and treated in

    the first instance, this apparent movement is unlikely to occur.If there is not a rapid initial response to treatment, after say two or three sessions,the therapist must consider the possibility that:

    (1) The key MTrP has not been correctly identified and treated(2) The diagnosis of MTrP pain is incorrect(3) There are factors causing persistence of the treated MTrP which have been

    overlooked.

    The latter is the most likely cause of treatment failure if the initial assessment was

    performed by an experienced clinician. Persistent biomechanical stress is likely to bethe most prevalent factor, but psychological stress with increased muscle tension,particularly affecting the neck and shoulders, is also very common. Less commonfactors include borderline hypothyroidism103 and a host of other endocrine, metabolicand nutritional inadequacies. Whilst these factors have been suggested by empiricalobservation and remain to be validated, a working knowledge of the most commonis essential to clinicians treating myofascial pain. Simons detailed account of perpetu-ating factors is recommended for reference,28 and Gerwin has provided an update onthis subject recently.104

    Caution

    In the authors perceptions there appear to be a number of conditions that fall into thegrey area between the clear cut myofascial pain syndrome affecting a single muscle and

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    the widespread involvement of the soma in fibromyalgia. A typical presentation hasfeatures of both and often appears to be a more complex version of the former. Usu-ally limited to a single quadrant of the body, unlike fibromyalgia, there is a generalisedtenderness of soft tissue compared with the unaffected side. This might representa myofascial pain syndrome with an abnormal degree of central sensitisation in theaffected segments on one side of the spinal cord. Whatever the pathogenesis, these

    conditions are difficult to treat and direct somatic stimulation of the tender pointsor MTrPs should be avoided, at least initially.

    SUMMARY

    The myofascial trigger point pain syndrome is a prevalent cause of regional pain anddysfunction. Good clinical skills in muscle palpation are needed to reliably identifythe myofascial trigger points (MTrPs) from which the pain emanates. The commonmanifestations of this syndrome can be identified and treated with limited training,but the more complex and esoteric presentations require detailed knowledge of func-tional anatomy and factors that perpetuate the condition.

    The pathophysiology of MTrPs is slowly becoming apparent. They appear to belocated in the endplate zone of the affected muscle fibres, where there is increasedspontaneous electrical activity, and signs of peripheral sensitisation of sensory nerves,as well as the appearance of contractures.

    Myofascial trigger point pain appears to respond well to therapies targeted at theMTrPs, although there is a lack of rigorous evidence confirming specific efficacy of themost popular therapies. Needling therapies, including injection techniques, are amongthe most popular interventions used by physicians and it seems clear that any effect ismediated via the needle rather than the injected substance. There are many physicaltherapies that are used in the management of myofascial pain and the majority involvethe application of pressure or stretch or both at the relevant MTrPs.

    Practice points

    Diagnosis of myofascial trigger point (MTrP) pain syndrome:

    Provocation of recognised pain by applying pressure to a point of tenderness ina taut band of skeletal muscle is the most reliable clinical feature of MTrP pain

    syndrome Examination for taut bands requires skilled palpation with the fingertips drawn

    across the muscle, perpendicular to the fibre direction

    Methods of alleviating myofascial trigger point pain:

    The main interventions used are needling or injection, which is directed at therelevant MTrPs, and physical therapies, which principally involve the applicationof pressure and stretch

    Needling appears to work without the need for injection and irrespective of

    the injected substance, but specific efficacy of needling has yet to be confirmed Stretching techniques can be taught to patients for self-management of myofas-

    cial pain and may be particularly useful for preventing or treating recurrence

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