Best Practice & Research Clinical Rheumatology Vol. 21, No. 2, pp.

367e387, 2007
doi:10.1016/j.berh.2006.12.006 available online at http://www.sciencedirect.com

9 Regional myofascial pain: diagnosis and management

Mike Cummings *
Medical Director 5 Lime Terrace, London W7 3HE, UK

Peter Baldry
Emeritus Physician Millstream House, Old Rectory Green, Fladbury, Pershore, Worstershire WR10 2QX, UK

This chapter denes and describes the condition that is known by the term myofascial trigger point pain syndrome. An outline is given of the current state of knowledge of the pathophysiology 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 terms and the reliability of the clinical diagnosis is discussed. The clinical evidence for and against the common therapeutic interventions used in the management of myofascial pain is reviewed in detail and some tentative conclusions are reached with respect to needling therapies. Key words: myofascial pain; myofascial trigger point; needling therapy; physical therapy.

INTRODUCTION Denitions The term regional myofascial pain is used clinically in at least two distinct ways. First it is used synonymously with the terms myofascial pain syndrome and myofascial trigger point pain syndrome to describe the specic clinical manifestation of a rather ubiquitous form of muscle pain that is derived from myofascial trigger points and which can be associated with a number of other sensory, motor and autonomic phenomena. Secondly,

* Corresponding author. Tel.: 44 2085799607. E-mail address: mike.cummings@btinternet.com (M. Cummings). 1521-6942/$ - see front matter 2006 Elsevier Ltd. All rights reserved.

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the term regional myofascial pain is used by clinicians to refer to soft tissue pain in general, particularly in circumstances where a more specic diagnostic category, such as tendinopathy or enthesopathy, is not apparent. This chapter is concerned with the more specic 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 t person for centuries remained an enigma and, as a consequence of this there was for long no general agreement as to what to call the underlying disorder. Guillaume de Baillou (1538e1616), when Dean of the medical faculty at the University of Paris, introduced the term muscular rheumatism for it. At the beginning of the 19th century two British physicians Balfour1 and Scudamore2 expressed the opinion that the pain arises as a result of inammation developing in the brous connective tissue in skeletal muscle. A view that continued to prevail in Britain throughout that century and one that was to lead Sir William Gowers, in 1904, during the course of a lecture, given at what was then called the National Hospital for the Paralysed and Epileptic, London, to conclude that as muscular rheumatism develops as a result of inammation of the brous tissue in muscle we may conveniently follow the analogy of cellulitis and term it brositis.3 This name was then widely employed for some years but once it became evident that there were no convincing histological changes to support the hypothesis the term was eventually abandoned and replaced by the non-committal one of myalgia. The evolution of present day concepts It was the French physician Francois Valleix who, in 18414, was the rst to observe that the pain in this disorder emanates from well dened focal points of tenderness and 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 at these sites are in a state of hyperactivity because of the effect on them of such factors as altered weather conditions, physical exertion and emotional upsets. It may, therefore, be seen that by the beginning of the 20th century some of the more enlightened physicians had come to appreciate that what hitherto had been variously called either muscular rheumatism or brositis occurs as a result of the development of increased activity in nerve endings at specic points of tenderness. A view endorsed by Sir William Osler who, in the 1909 edition of his textbook The Principles and Practice of Medicine6, when discussing the disorder, stated it is by no means 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 view began to appear. One of the rst clinicians to provide this was Hunter, a physician in Canada who, in 1933, described cases in which abdominal pain emanated from points of tenderness in anterior abdominal wall muscles.7 Then in 1936, Edeiken & Wolferth, physicians at the University of Pennsylvania Medical 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 rm pressure to points of exquisite tenderness in muscles around the scapula.8 The physician, however, who during the 1930s made the greatest contribution to our knowledge concerning the pathophysiology, diagnosis and treatment of what, currently, is called the myofascial trigger point pain syndrome was John Kellgren during the 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 rst carried out an experiment on healthy volunteer medical students. In this they injected pain-evoking hypertonic saline into muscles and observed that rather than the pain being experienced at the injection site it was felt some distance away at what they called the zone of pain referral. Kellgren then turned his attention to patients with muscle pain.9 With respect to these he said: A number of cases of brositis or myalgia have been investigated. The distribution of pain from normal muscles guided me to the muscles from which spontaneous pain may have arisen. Such muscles always presented tender spots on palpation and pressure on these spots reproduced the patients pain. He then went on to conrm that the pain arose as a result of nerve hyperactivity at these tender points by showing that it could be alleviated, often for several days, by injecting 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 study of muscle pain was not renewed. Fortunately, however, during the 1940s, a young American physician, Janet Travell, decided to take up the study of the subject where he had left off. She did so having read how Kellgren had shown that widespread dull aching pain in muscle emanates from what an American orthopaedic surgeon had aptly called trigger points. Travells study of the subject led her to realise that pain in the disorder that hitherto had variously been called rheumatism, brositis, myalgia and a host of other synonyms arises not only from skeletal muscle itself but also from its brous 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 specic pattern of myofascial trigger point pain referral and over the years, together with her colleague David Simons, published diagrams of these in two prestigious publications.10,11 Prevalence of myofascial trigger points Myofascial trigger points (MTrPs) are recognised by many clinicians to be one of the most 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 of young, asymptomatic military personnel12 and with a similar prevalence in the masticatory muscles of a group of unselected student nurses.13 Active MTrPs, those causing spontaneous pain, have been diagnosed as the primary source of pain in 74% of

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Figure 1. These diagrams illustrate some of the more common myofascial trigger point sites (#) in the head and neck and their respective pain patterns.

96 patients with musculoskeletal pain seen by a neurologist in a community pain medical centre14 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 neck pain, 55% were found to have active myofascial trigger points as the cause of their pain16, as were 30% of those presenting with pain to a university primary care internal medicine group practice from a consecutive series of 172 patients.17 A study of musculoskeletal disorders in villagers from rural Thailand has demonstrated myofascial pain as the primary diagnosis in 36% 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

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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.

 A local twitch response (LTR) within the band of muscle on plucking palpation across the bres. Various classications have been used for different presentations of MTrPs, but the most straightforward has been alluded to above. That is the distinction between active and latent MTrPs. Active MTrPs are classied as those that cause spontaneous pain, while latent MTrPs have all the same clinical features without being responsible for a 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 zone is where the motor nerve, on entering a muscle, divides into a number of branches with each of these having a terminal claw-like motor endplate embedded in the surface of a muscle bre.

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Each MTrP contains a neurovascular bundle. The principal contents of this are motor nerve endings and group III and IV nociceptive sensory afferent nerve endings.19,20 Sensory phenomena Tenderness has been investigated using pressure algometry and several studies have demonstrated that this is a reliable tool for assessing MTrP sensitivity.21e23 Bendtsen et al investigated the nociceptive process in the MTrP pain component of 40 cases of chronic tension-type headaches compared with 40 healthy controls.24 The relationship between the pressure applied over an MTrP and the associated pain was found to be linear e that is increments in pressure were proportional to the resulting increments in pain. Over normal muscle the relationship was found to be non-linear; typically increments in pressure over normal muscle do not cause pain until a threshold is reached, beyond which pain increases disproportionately. The authors therefore postulated that myofascial pain is mediated by low-threshold mechanosensitive afferents projecting to sensitised dorsal horn neurons. Motor phenomena Whilst taut bands have been detected in muscle for a very long time25, the precise nature of the MTrP has remained elusive. It is only relatively recently that a pathophysiological marker, in the form of spontaneous needle EMG activity, has been identied within 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 the vicinity of an active MTrP, but only the continuous low amplitude action potentials could be recorded from latent MTrPs. There has been controversy over the likely site of origin of this electrical activity. Hubbard & Berkoff postulated that the source was intrafusal bres within the muscle spindle26, but Hong & Simons have put forward a strong argument in favour of dysfunctional motor endplates.27 It is unfortunate that this type of electrical activity is not specic to MTrPs and can be demonstrated in the endplate zone outside an MTrP, although it has not been demonstrated outside the endplate zone.28 Spontaneous electrical activity (SEA) e referring to the continuous low amplitude action potentials e has been shown to vary signicantly in amplitude between symptomatic patients (suffering from tension headaches and bromyalgia) and control subjects.26 In normal subjects with latent MTrPs, SEA recorded from the upper trapezius has been shown to increase dramatically in amplitude as a result of psychological stress alone;29 and phentolamine, an alpha adrenergic blocker, appears to diminish the amplitude and frequency of spikes recorded from MTrPs in humans30 and in a rabbit model.31 The local twitch response (LTR) has been studied electrophysiologically in both man and the rabbit model.27 The muscle contraction of an LTR appears to occur only within the taut band and the latency of the contraction following direct mechanical stimulation of the MTrP is consistent with a polysynaptic reex. LTRs can be abolished by a local anaesthetic block, or by transection of the innervating nerve, and are diminished following cord transection, although they recover almost completely after the period of spinal shock.27 et al have contributed important work with MTrPs in the infraspinatus Couppe muscle 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 blind the examiner. Around both points 20 concentric needle electromyographic (EMG) recordings were obtained at rest. More subjects had spontaneous EMG activity at the MTrPs than at the control point. The EMG activity was interpreted as end-plate noise or spikes or both. The MTrP Root Mean Square amplitudes were signicantly higher than at the control points. This is the rst work to conrm 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 demonstrates a reduction in amplitude of SEA at what is considered to be the equivalent of MTrPs following therapeutic-style dry needling. This is soft evidence for the apparent immediate benet of needling in myofascial pain that is reported by clinicians in practice. Biopsy studies Simons28 suggests that highly contracted portions of muscle bres, which he calls contraction knots, may be a specic histological marker for the MTrP (Figure 3). They rten (muscle indurations)34 were rst described in 1951 in biopsies of Muskelha and again in 1960 in biopsies from similar sites in patients described as having brositis.35 In 1976 MTrP criteria were used to investigate canine muscle and sites that were clinically equivalent to MTrPs in humans were examined histologically.36 Muscle crosssections revealed some darkly staining, large, round bres. The equivalent longitudinal appearance showed central bulges within some muscle bres where there was a highly contracted portion. Either side of this bulge the bre 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 bres. Note that in a normal muscle bre (NMF) the sarcomeres are of equal length, but in a muscle bre 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 histological ndings have been conrmed and further elaborated, with the use of electron microscopy, on biopsies of human gluteus medius MTrPs from fresh cadavers.37 Since the demonstration of SEA from MTrPs, Simons has proposed that the contraction knot is likely to be the source of this activity.38 He cites experimental research on mammalian skeletal muscle39 and the microscopic appearance of a contraction knot in canine gracilis muscle36 to support his contention that the contraction knots observed in MTrP biopsies occur at the site of the motor endplate. He adds further support to this suggestion by observing that the longitudinal dimension of these knots is similar to the length of a motor endplate. In 2000, De Stefano et al performed a slightly different type of biopsy study of MTrPs. They used immunohistochemistry to study substance P immunoreactive (SP-ir) nerve bres in muscle biopsies from the upper trapezius of nine women with myofascial pain, nine women with bromyalgia (FM) and nine healthy women.40 They found no difference in numbers of SP-ir nerve bres in the three groups of women, but there were signicant differences in the mean optical density of SP-ir nerve bres, i.e. there were differences in terms of the quantity of substance P (SP) in the nerve bres. SP may be taken as a marker for peripheral sensitisation, so it is interesting to note that SP concentration was signicantly greater in MTrP biopsies from myofascial pain patients compared with FM patients, and SP concentration was signicantly 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 ne, non-cutting needle (an acupuncture needle) as the basis for the development of a microdialysis instrument to measure the in vivo biochemical milieu of muscle in near realtime at the sub-nanogram level of concentration. They used nine volunteers: three normal, three with latent MTrPs in upper trapezius and three with active MTrPs in upper trapezius. Concentrations of protons, bradykinin, calcitonin gene-related peptide (CGRP), substance P (SP), tumour necrosis factor alpha, interleukin-1beta, serotonin and noradrenaline were found to be signicantly higher in the active group than either of the other two groups (P < 0.01). pH was signicantly lower in the active group than the other two groups (P < 0.03). After the needle was moved to obtain an LTR, a manoeuvre that is thought to be associated with therapeutic benet, the concentrations of CGRP and SP in the active MTrP sites diminished signicantly. This is rather preliminary work, in a small number of subjects, but it may be an important step towards a fuller understanding of the elusive substrate of this apparently 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. This may be brought about either by a direct injury to the muscle or by the sudden or repeated overloading of it. Alternatively, it may develop when the muscle is subjected to 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 temperament holds a group of muscles in a persistently contracted state. Muscle wasting MTrP activity is liable to develop when muscles have become weakened and wasted by malignant disease or a neurological disorder. With respect to strokes, MTrP nociceptive pain is liable to develop when weakened muscles become overloaded during attempts to restore movements to them during the recovery stage. Muscle ischaemia MTrP activity may arise when, because of arterial obstruction, the muscles of a limb become ischaemic. Visceral pain referral Pain arising as a result of visceral disease is frequently referred to both skin and muscles. When this happens MTrPs in muscles situated in this zone of pain referral are 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 spondylosis or disc prolapse, pain may also arise as a result of the secondary development of TrP activity in the paraspinal muscles.43 Climatic causes MTrPs are liable to become active when the muscles containing them are exposed to adverse environmental conditions such as damp, draughts, excessive cold or extreme heat.44 DIAGNOSIS OF MTrP PAIN SYNDROME Clinical manifestations Patient history Pain. This is by far the most common presenting complaint. Typically the pain is described as deep, aching and poorly localised. It is usually restricted to one quadrant of the body, although complex patterns from multiple MTrPs may give a wider distribution. It is important to determine the precise nature and pattern of the pain, as would be done when taking a standard medical history. Paraesthesia is not uncommon in association with the pain and often conrms in the patients mind the false impression that they have 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 nd 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 developed to 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 an extremity. MTrPs appear to affect proprioceptive function. In the cervical musculature, in particular sternomastoid, this may be responsible for dysequilibrium, even to the extent that the patient may describe true vertigo. In the limb musculature this may result 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 often aggravates 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 faster to repair, so less likely to develop or sustain active MTrPs. By comparison, the musculoskeletal system of the middle-aged adult is becoming increasingly degenerate, less resilient and slower to heal. In general the middle-aged are less active, but engage in unaccustomed bouts of physical activity. They tend to suffer most with the pain of active MTrPs. Latent MTrPs can be found in the majority of elderly people, causing stiffness and reduced active range of movement, but this age group present less frequently with the pain of active MTrPs. Sex. Women seem to present more frequently with myofascial pain than men. It has not been established whether myofascial pain is more common in women, or whether they are more likely to present with this type of pain. It is certainly true that phenotypic differences can inuence biomechanical loading and, for the same mass, women tend to have wider hips and narrower shoulders than men. Biological factors such as these may be important, but socio-economic differences in terms of working environments may also have an inuence. For example, a higher proportion of the male workforce performs physically strenuous jobs and it has been noted that these individuals suffer less from myofascial pain than sedentary workers. Examination ndings Tender point. This is the key feature of an MTrP, although it is clearly not exclusive to MTrPs. A tender point is usually a discrete area in the soma, which, when pressure is applied to it, produces more pain than its immediate surroundings. In a clinical setting, pressure is usually applied with the ngertips onto the surface of the body. The pressure is transmitted through a range of soft tissues that are compressed between the examiners ngertips and an unyielding surface beneath. The latter is often bone, but may 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 of inconsistency in the unyielding surface beneath. Pressure applied to these areas is concentrated over a small volume of soft tissue, rather than distributed more widely and evenly to the surroundings. Thus consistent extrinsic pressure, whether applied with ngertips or an algometer, generates greater pressure within the soft tissues at these sites 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 myofascial pain syndrome, active MTrPs are rarely symmetrical, as opposed to bromyalgia, in which 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 the muscle layer whilst palpating, or to get the patient to perform an isometric contraction whilst putting pressure over the tender point. Both of these techniques tend to increase the relative pressure in the muscle layer and, therefore, have some discriminative value. Taut band. The taut band associated with an MTrP is palpated by drawing the ngertips of the examining hand forward and back perpendicular to the bres of the relevant muscle. The muscle should be placed on a slight stretch and the skin and subcutaneous tissues are moved with the ngertips as the muscle bres are palpated. Some supercial muscles can be palpated between nger and thumb in a pincer grip and the taut band is felt as the bres are allowed to slip between the palpating digits. The latter technique often requires the relevant muscle to be slackened off. Pain. As an active MTrP is palpated, the patient will often exclaim thats it, or give a similar verbal indication that they recognise the pain. The pain is usually sufcient to cause the patient to give an involuntary jerk, withdrawing slightly from the palpating ngers. This is referred to as the Jump Sign. It is very import to ask the patient if it is their usual pain that is generated by applying pressure to the MTrP and to ask them to indicate the pattern of pain produced. The pain referral patterns produced by MTrPs in skeletal muscle are frequently characteristic of the specic muscle and, with experience, the musculoskeletal specialist can determine the most likely muscles involved from the history alone, so that detailed examination can be targeted to the relevant areas. Local twitch response. When the palpating nger is snapped across the taut band of an active MTrP, there is often a detectable contraction of it (Figure 4). This local twitch can be visible if the muscle is supercial, or may be felt by the examiner. The LTR is more frequently encountered when directly needling the MTrP. Other examination ndings. MTrPs invariably cause shortening of the affected muscle and may cause a reduction in power without muscle atrophy. Muscle shortening results 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 to measure the relevant ROM in a clinical setting. Assessment of power is generally

Figure 4. This gure illustrates the examination of a muscle for trigger points by snapping palpation across the bres to elicit a local twitch response. The image on the right shows a local twitch within the bres 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 test power, resisted muscle contraction, often causes pain if the muscle tested is harbouring an active MTrP, especially if the resistance is applied with the muscle in a shortened position. Reliability of clinical features There have been several studies testing the inter-observer reliability of the examintion for 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 the examiners underwent a 3 hour period of training.48 The following clinical features tested are placed in order of overall inter-rater reliability: (1) (2) (3) (4) (5) Pain recognition Taut band Tender point Referred pain LTR.

In 2001, Sciotti et al took this work further by demonstrating that two trained examiners, blind to each others ndings, can reliably localise latent MTrPs in upper trapezius with a precision that essentially approaches the physical dimensions of the clinicians own ngertips.49 Simons recommends that the minimum acceptable criteria for diagnosing a myofascial TrP are the combination of spot tenderness in a palpable band of skeletal muscle and subject recognition of the pain, but he admits that palpation of a taut band is conditional 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 global terms. This is because of the use of acupuncture in the East. Acupuncture is also popular 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 innocuous physiological 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, that the nature of the injected substance makes no difference to the outcome and that there is no therapeutic benet in wet over dry needling.50 These conclusions were supported by all the high quality trials in the review.51e59 The authors of the review concluded: The hypothesis that needling therapies have specic efcacy in the treatment 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 the needle, rather than from either, an injection of liquid in general, or any substance in particular. All groups in the review in whom trigger points were directly needled showed marked improvement in their symptoms; therefore further research is urgently needed to establish the specic effect of trigger point needling, with emphasis on 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. There is, perhaps, a little more weight in favour of there being a specic effect of needling61,63,64, but this is far from denitive. It does seem quite clear now, however, that botulinum toxin 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 antagonist tropisetron for injection into MTrPs,72 following the demonstration of its efcacy when administered systemically in patients with bromyalgia.73 It has yet to be tested in a RCT of myofascial pain, but it may turn out to be the rst substance that provides more benet 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 may have 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 undetermined. Despite the fact that a causal relationship has not been established between direct needling of trigger points and improvement in symptoms, a discussion of the potential mechanisms involved may still be useful in developing future research questions. 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 therapeutic factor in both techniques is mechanical disruption by the needle.28 The common factor is certainly needle insertion into the trigger point; however, Hong has demonstrated the importance of stimulating a LTR in achieving an immediate effect,74 and, with Simons, cites evidence that the LTR is mediated by a segmental spinal reex.27 Fine et al performed a rigorous experimental study, in which trigger points were subject to direct wet needling, and clearly demonstrated that an opioid mechanism was involved in trigger point pain relief.75 In view of this evidence, combined with the apparent clinical effectiveness of supercial dry needling (a technique that does not involve direct penetration of the MTrP),76 it seems possible that the needle can work through sensory stimulation as well as through mechanical disruption and this would 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 in clinical practice are probably physical treatments. Whilst they are given many different titles, most involve the application of some form of mechanical pressure to the MTrP or stretch of the affected muscle, or both. Travell developed the technique of stretch and spray.10 This involves the use of a vapocoolant spray applied in a dened pattern just prior to stretching the involved muscle. The sudden sensory stimulus of the spray acts as a distraction and reduces the discomfort from stretching a muscle shortened by an MTrP. Various other techniques have been described to enhance stretching.

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Post-isometric relaxation78 and reciprocal inhibition28 involve voluntary muscle contraction by the patient of the target muscle or its antagonists, respectively. Accessory techniques, including phased respiration and eye movements, can also be used to augment stretching. Pressure has been applied to TrPs in the form of ischaemic compression, shiatsu, acupressure, pressure release and many forms of massage. Simons gives 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 ve patients with bilateral active MTrPs in trapezius, Jaeger & Reeves randomly selected the side for treatment with stretch and spray and demonstrated a signicant reduction in MTrP sensitivity (pressure pain threshold measured with an algometer) compared with the untreated side.79 Pain scores decreased signicantly but did not correlate with MTrP sensitivity. Gam et al performed a randomised controlled trial comparing ultrasound, massage and exercise with sham-ultrasound, massage and exercise with a 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 treatment groups improved signicantly compared to the control, but the latter was inadequate to conclude that massage and exercise had a specic effect. Interestingly, a much higher intensity ultrasound treatment (referred to as high-power, pain-threshold, static ultrasound) has subsequently proved to be more effective than conventional ultrasound, 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 have exceeded the negative.87 A systematic review published in 1992 concluded that laser therapy appears to have a substantial specic therapeutic effect.88 However, a plausible mechanism is still lacking as there is no sensory stimulation perceived from active LLLT and the photon beam has very limited penetrance. Moreover, experimental work by Lundeberg has demonstrated that this type of laser stimulus has no demonstrable effect on 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 intensity TENS was effective in reducing myofascial pain but not MTrP sensitivity. In view of this it is not surprising that in a trial 9 years later of sub-threshold TENS applied to patients with myofascial pain and dysfunction of the masticatory system, the active intervention proved no better than the sham.91 Electrical stimulation over MTrPs with a pocketsized stimulator has been shown to increase pain threshold algometer readings over the treated points compared with a no treatment control,92 but whether this would correlate to clinically signicant symptom relief has not been established; furthermore, Jaeger & Reeves have indicated that there may be no correlation between pain reduction 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 sufcient to induce muscle contraction. A third group received a sham control. Sixty patients were randomised to the three groups. 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 pain of 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 myofascial pain related to temporomandibular joint dysfunction,98 but benzodiazepines are not suitable for lengthy treatment because of the risk of dependence. More unusual treatments involve mud baths and magnetic elds. According to a randomised controlled trial by Pratsel et al, mud baths containing sulphur compounds reduce the sensitivity of MTrPs compared to those that do not contain sulphur compounds.99 Pain scores in post-polio patients reduced signicantly resulting from the application of 300e500 Gauss magnetic devices to their pain trigger points, compared with the use of placebo devices.100 More recently a different form of magnetic stimulation (peripheral repetitive magnetic stimulation e rMS) has shown benet beyond control in trapezius MTrPs.101 Prognosis Despite the lack of convincing evidence of specic efcacy for any of the therapies regularly applied to MTrPs, the empirical experience of clinicians treating myofascial pain is very positive. Simple clinical audit suggests that the majority of people get better with dry needling,102 and the same probably applies to the popular non-needling physical therapies. As a general rule, myofascial pain syndromes which have been present for 6 months or less appear to be curable, but those which have been present for longer, or have followed a chronic relapsing course, can only be treated symptomatically, 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 movement rather than actual movement of a specic MTrP and can occur as a result of treatment of a series of satellite MTrPs. If the key MTrP is identied and treated in the rst 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 identied 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 be the most prevalent factor, but psychological stress with increased muscle tension, particularly affecting the neck and shoulders, is also very common. Less common factors include borderline hypothyroidism103 and a host of other endocrine, metabolic and nutritional inadequacies. Whilst these factors have been suggested by empirical observation and remain to be validated, a working knowledge of the most common is essential to clinicians treating myofascial pain. Simons detailed account of perpetuating factors is recommended for reference,28 and Gerwin has provided an update on this subject recently.104 Caution In the authors perceptions there appear to be a number of conditions that fall into the grey area between the clear cut myofascial pain syndrome affecting a single muscle and

382 M. Cummings and P. Baldry

the widespread involvement of the soma in bromyalgia. A typical presentation has features of both and often appears to be a more complex version of the former. Usually limited to a single quadrant of the body, unlike bromyalgia, there is a generalised tenderness of soft tissue compared with the unaffected side. This might represent a myofascial pain syndrome with an abnormal degree of central sensitisation in the affected segments on one side of the spinal cord. Whatever the pathogenesis, these conditions are difcult to treat and direct somatic stimulation of the tender points or MTrPs should be avoided, at least initially. SUMMARY The myofascial trigger point pain syndrome is a prevalent cause of regional pain and dysfunction. Good clinical skills in muscle palpation are needed to reliably identify the myofascial trigger points (MTrPs) from which the pain emanates. The common manifestations of this syndrome can be identied and treated with limited training, but the more complex and esoteric presentations require detailed knowledge of functional anatomy and factors that perpetuate the condition. The pathophysiology of MTrPs is slowly becoming apparent. They appear to be located in the endplate zone of the affected muscle bres, where there is increased spontaneous 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 the MTrPs, although there is a lack of rigorous evidence conrming specic efcacy of the most popular therapies. Needling therapies, including injection techniques, are among the most popular interventions used by physicians and it seems clear that any effect is mediated via the needle rather than the injected substance. There are many physical therapies that are used in the management of myofascial pain and the majority involve the 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 in a taut band of skeletal muscle is the most reliable clinical feature of MTrP pain syndrome  Examination for taut bands requires skilled palpation with the ngertips drawn across the muscle, perpendicular to the bre direction Methods of alleviating myofascial trigger point pain:  The main interventions used are needling or injection, which is directed at the relevant MTrPs, and physical therapies, which principally involve the application of pressure and stretch  Needling appears to work without the need for injection and irrespective of the injected substance, but specic efcacy of needling has yet to be conrmed  Stretching techniques can be taught to patients for self-management of myofascial pain and may be particularly useful for preventing or treating recurrence

Regional myofacial pain 383

Research agenda  Novel microdialysis work may indicate a fruitful area for further investigation in attempts to uncover the pathophysiology of the rather elusive myofascial trigger point  Further clinical studies are needed to conrm the specic efcacy of the most commonly used interventions

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