Physical Therapy in Sport 5 (2004) 2–12 Myofascial trigger points: the current evidence Centre for Sports Medicine Research and Education, University of Melbourne, 300 Berkeley Street, Parkville, Vic., Australia Received 10 November 2003; revised 17 November 2003; accepted 18 November 2003 This paper provides an overview of the current state of knowledge regarding the history, pathophysiology, mechanisms of pain production, and proposed methods of treatment of myofascial trigger points. Despite the increasing body of published literature on this subject, manyfundamental questions remain unanswered. This paper aims to give the therapist a greater understanding of the current knowledge ofmechanisms of muscle pain, treatments that have been shown to be effective, and the ways in which these treatments may produce theireffect. Most effective treatments have at their core a form of counter-stimulation or application of a second noxious stimulus. It remainsunclear if it is this counter-stimulation or more specific elements of muscle stimulation that are the active ingredients, but it is possible thateach contributes to effective outcomes.
q 2003 Elsevier Ltd. All rights reserved.
Keywords: Myofascial trigger points; Counter-stimulation; Evidence-based medicine quite trivial when assessed. It is not clear whether thepsychological disturbance seen in these patients is a part of Although myofascial trigger points are a widely the pathology or merely reactive to the chronic pain state.
recognised phenomenon in clinical practice, there remains Importantly, psychological disturbance, from whatever much to be elucidated with regards to their pathophysiol- cause, will impact on a patient’s interpretation of pain ogy, mechanisms of pain referral, and treatment of choice.
From the outset, it must be noted that much of the early literature on trigger points, myofascial pain, and fibromyal- As trigger points can also occur in the absence of pain gia was based on anecdotal reports and the clinical syndromes, this paper aims to address the current state of experience of those using this form of treatment. Most knowledge with respect to trigger points as an isolated popular beliefs are based on theories generated on this basis, phenomenon, rather than addressing treatment approaches and it is only in recent times that a more scientific approach to defining and treating the phenomenon of myofascial Trigger points can be seen in the setting of occupational trigger points has developed. Despite this increasing or athletic injury due to muscle imbalances, postural interest, much of the fundamental understanding remains deficiencies, or secondary to another underlying pathologi- based in the theories of the early clinicians and still requires cal process. Examples of the latter include trigger points in quadratus lumborum in association with an irritated lumbar Trigger points are most often discussed in the setting of disc, or gluteal trigger points in the presence of hip joint myofascial pain syndromes, in which widespread or pathology. Desk workers may present with headaches that regional muscular pain is associated with hyperalgesia, are reproducible with pressure over trapezius trigger points psychological disturbance, and significant restriction of due to the prolonged muscle contraction in inappropriate postures, or the development of thoracic spine stiffness. It is these syndromes recall an inciting factor for their pain, important to assess for and treat any precipitating or however, some may not. Inciting factors may often seem perpetuating factors in the presence of trigger points inorder to maximise the chance of a long-term response to any * Tel.: þ61-3-8344-4118; fax: þ 61-3-8344-4188.
E-mail address: [email protected] (L.K. Huguenin).
1466-853X/$ - see front matter q 2003 Elsevier Ltd. All rights reserved.
doi:10.1016/j.ptsp.2003.11.002 L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 Early writings on trigger points and their treatment were In summary, the diagnosis of trigger points relies on sporadic and lacked uniformity of diagnostic criteria. The finding a local tender spot within a taut muscle band, reproduction of recognisable symptoms, and a local twitch response to snapping palpation or needle insertion.
reference for those involved in treating this condition. The There are, however, several caveats to bear in mind when theories of pathogenesis contained within this volume have establishing examination findings, not the least of which is subsequently been challenged, but never conclusively the lack of a gold standard for assessment of trigger points.
disproved and the definition of trigger points presented is This lack of standardised assessment makes validity studies still the most widely used in clinical practice.
near impossible, although reliability trials have beenperformed. examined patients withchronic myofascial pain or fibromyalgia, and the most common finding in their subjects was local tenderness andtaut muscle bands. Reliability of examination for taut bands, The classical and most commonly used description of muscle twitch, and active trigger points, however, was Travell and Simons define trigger points as In a blinded trial of physiotherapists experienced in the presence of exquisite tenderness at a nodule in a treating lower back pain ), the reliability of palpable taut band (of muscle). Trigger points are able to assessment for the presence of three trigger points described produce referred pain, either spontaneously or on digital by Travell and Simons was poor and it was noted that issues compression. The clinical definition came to be that trigger as simple as patient positioning, palpation technique, and points are localised areas of deep tenderness within a taut the amount of force applied significantly influenced results.
band of muscle. They exhibit a local twitch response Of interest, reliability was not improved when the sample (muscle fasciculation) or jump sign (whole body move- was reanalysed for only those therapists reporting the use of ment) in response to digital pressure or dry needling. In their trigger point examination in their routine practice.
common trigger point locations and their referral zones.
inter and intra-rater reliability, using two highly trained These locations have been noted to have significant examiners for assessment of the presence and number of similarities to acupuncture points used in traditional trigger points in asymptomatic patients, was poor. In a study of four clinicians together resulted in improved reliability of Two main types of trigger points are described. Active identification of trigger points. In a study by trigger points are those that may be responsible for the , it was reported that localisation of trigger points was presenting pain complaint. They may also be associated unreliable in untrained examiners, and only marginally with less readily definable symptoms such as weakness, more reliable in trained examiners. Further, parasthesia, or temperature changes, and they may have found that taut band and local twitch responses could associated referred pain. Latent trigger points present with not be reliably assessed, and examination for referred pain muscle shortening, and pain occurs only on the application had low reliability when extensive training had been of external pressure. These trigger points may become undertaken, but was not at all reliable without this. Another activated by a variety of stimuli, including poor posture, study has shown moderate reliability for the presence of local tenderness and production of recognised pain, but poorreliability for twitch responses and the production ofreferred pain ( On palpation of a muscle, a trigger point is recognised as a local tender spot within a taut muscle band. If a triggerpoint is active, the patient will recognise the symptoms Currently, there is no gold standard pathological test for produced when pressure is applied to it. Latent trigger points the identification of trigger points. Therefore, much of the will be painful on palpation, but the sensations will not be research into the pathophysiology of trigger points is recognisable. A local twitch response has been described in directed towards indirectly verifying the common theories response to ‘snapping palpation’ of the taut band, and to the for their formation. Histological studies have been incon- clusive, with either non-specific changes of fibrosis and palpation is described as similar to plucking a guitar string.
absence of inflammatory cells, or negative findings ( The fingers are placed over the trigger point and then Imaging of trigger points has not been shown to quickly snapped back over the muscle at right angles to the L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 One study that used biopsy indicated that there may be phosphates were reduced and low energy phosphates altered levels of high energy phosphates in painful muscles increased at trigger point sites in patients when compared to non-tender muscle points in both patients and controls this has led to some promising pilot trials on the use of 31P NMR which can assess the levels of different forms of metabolic derangement at trigger point sites. However, phosphate within the muscle. 31P NMR is a form of nuclear lactate and pyruvate are the products of anaerobic muscle magnetic resonance spectroscopy that can quantify relative metabolism, and their levels were not increased. Therefore, amounts of different phosphate compounds in tissues, as although a pure ischaemic cause is unlikely, there is some each compound is at a different energy state. Phosphate evidence to suggest a metabolic abnormality at trigger point compounds (e.g. ATP, phosphocreatine) in muscle are sources of energy, and quantification could assist inassessing the metabolic status of the muscle. Unfortunately, to date, there is no clear indication of the pathologicalchanges to be expected in myofascial pain.
The energy crisis theory could well co-exist with the motor end plate hypothesis. The motor nerve synapses witha muscle cell at the motor endplate. Needle EMG studies have found that each trigger point contains minute loci thatproduce characteristic electrical activity ( The aetiology of trigger points is not clear, but the two most widely accepted theories (energy crisis theory and motor endplate hypothesis), when combined, provide a The endplate noise seen on EMG is thought to plausible explanation. There is a third, yet to be experimen- represent an increased rate of release of acetylcholine (ACh) tally verified theory, which suggests the primary site of from the nerve terminal. A small amount of activity at the pathology to be the spinal nerve, with secondary muscle motor endplate is not enough to cause muscle contraction, changes occurring (). The more widely accepted but can result in action potentials being propagated a small theory is centred on the muscle cell and motor endplate distance along the muscle cell membrane. This small amount of propagation may be enough to cause activationof a few contractile elements and be responsible for some The energy crisis theory is the earliest explanation of 5.3. Radiculopathic model for muscular pain trigger point formation ). This theory postulates that increased Not all researchers agree with the theories of Travell and demand on a muscle (increased neural input), macrotrauma, Simons. Most opposing theorists postulate a neurological or recurrent microtrauma leads to increased calcium release cause as the primary stimulus and trigger points as a from the sarcolemma and prolonged shortening of the sarcomeres. Prolonged shortening compromises the circula- tion, with the subsequently reduced oxygen supply leaving muscular pain and states that ‘myofascial pain describes the cells unable to produce enough ATP to initiate the active neuropathic pain that presents predominantly in the process of relaxation. Ischaemic by-products of metabolism musculoskeletal system’ (p. 121). The radiculopathic accumulate (), being in part responsible for model is based on all denervated structures exhibiting some of the pain produced, by sensitisation and direct super sensitivity. From clinical observations, stimulation of sensory nerves. Unfortunately, there are no states that neuropathic nerves are most commonly found at studies to date that can confirm such muscle injury as the the rami of segmental nerves, and therefore represent a radiculopathy. If neural injury or compression and partial The concept of altered muscle metabolism underlying denervation are the site of origin of this pathology, he the changes at trigger point sites was investigated by believes that it helps to explain the lack of pathology seen in Bengtsson (1986). Muscle energy stores can be measured by muscle and the sensory, motor, and autonomic changes seen the levels of various phosphate containing compounds.
Adenosine triphosphate, phosphocreatine, and adenosine diphosphate are compounds capable of donating their relates to intervertebral disc degeneration with nerve root phosphate moiety and releasing energy for muscle activity.
compression or angulation due to reduced intervertebral Adenosine monophosphate and free creatine are the space and resultant paraspinal muscle spasm. This is remaining compounds after this process and are, therefore, described as a form of neuropathy. This neuropathy then low energy molecules. In a biopsy study of patients with sensitises structures in the distribution of the nerve root, fibromyalgia, it was found that the levels of high-energy causes distal muscle spasm, and contributes to other L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 degenerative changes in tendons and ligaments within its noise with extra ACh released in response to the needle distribution that are then perpetuated by the ongoing muscle shortening. Therefore, this theory is not only used to explain trigger point formation, but also conditions such as abnormal activity in normal subjects or in non-tender muscle points 1 cm from the trigger points, there remains Based on his theories, proposes that long controversy about the significance of this ‘characteristic’ lasting pain relief requires needle treatment to the shortened SEA. In rabbit muscle, this pattern of activity has been paraspinal muscles in order to reduce nerve root com- identified at trigger point sites, but not control sites, even pression, as well as to trigger points more local to the site of when the control sites were also located close to motor humans is a little more confusing. In an unblinded study on behind traditional trigger point teaching is circular and ten human subjects, endplate noise occurred in all muscles excludes the possibility of a non-muscular origin of the tested at clinically determined trigger points ( pathology. They suggest that the characteristics of the pain ). Such endplate noise, however, also occurred in from trigger points are not distinguishable from neural pain, endplate zones outside of trigger points in four muscles.
and that a primary neurological cause is a much more likely Taut bands outside of the endplate zone did not exhibit explanation for the local and referred sensations of endplate activity. The authors concluded that these myofascial pain. To date, no neurophysiological studies potentials are characteristic of, but not restricted to, trigger have confirmed or denied these claims. Routine nerve conduction testing has not identified any abnormalities, but EMG has been found to exhibit SEA in both patients with may be lacking the sensitivity to do so.
long-term myofascial symptoms and asymptomatic patientswith identified trigger points. In the study by , the onset of recorded EMG activity corresponded well to the subjects’ report of the onset ofpain with needle advancement.
A pattern of EMG activity said to be characteristic of SEA in trigger spots in rabbit muscle has been shown to trigger points was first described in human subjects by reduce after dry needling treatment when compared to a occurred more reliably if local twitch responses were observed in response to needle insertion. This finding termed spontaneous electrical activity (SEA), and has suggests that any effect of dry needling may be due to a subsequently also been confirmed in rabbit studies ( more complex mechanism than muscle trauma alone.
SEA is seen as low amplitude backgroundnoise (50 mV), with superimposed high amplitude spikeactivity (100 – 700 mV), in a resting muscle. Initially, this pattern of activity was postulated to represent stimulation ofintrafusal muscle spindle fibres, which are innervated by the As early as 1938, the production of characteristic patterns of local and referred muscle pain was described in response Other researchers have since claimed that it is more likely to to injection of hypertonic saline (Muscle pain is likely to be transmitted by Group III (A delta, thin ). The motor end plate theory states that the back- myelinated) and Group IV (c, non myelinated) afferent ground noise (motor endplate noise) represents excessive release of packets of ACh by the motor nerve terminal next to the muscle cell. ACh is a neurotransmitter, which causes mini depolarisations of the post-synaptic muscle cell membrane (). A muscle contraction requires a large amount of ACh release to initiate adequate ever, serotonin has been shown to increase muscle pain in depolarisation of the muscle membrane for propagation of healthy volunteers, but not subjects with myofascial pain an impulse. The spontaneous activity of normal motor endplates shows more discrete, random, and non-overlap- antagonist has not been shown to influence muscle pain ping electrical activity (known as mini endplate potentials), rather than the haphazard discharge that has been attributed be important in the increase in pain threshold after electrical to trigger points. Within this theory, the origin of the spikes seen in trigger point EMG is unclear. One suggestion is that pain has been positively correlated with muscle levels of they may represent propagated single muscle fibre action potentials occurring as a result of summation of background Although substance P and calcitonin gene related peptide L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 (CGRP) are important transmitters in the nerve endings in muscle, and also at the spinal cord, they are not directly that the phenomenon of referred muscle pain must have a central basis. It is thought that in a resting state, each dorsal horn neurone has a receptive field in the body from which it Muscle pain from the injection of capsaicin (a substance used for experimental pain production) has been shown to have applied stimuli to known receptive fields of be of lower intensity, but more likely to produce referral, specific dorsal horn neurons in rats and found that new either to skin or deeper structures when compared to receptive fields have opened for these neurons. That is, the intradermal injection of the same quantity and concentration neurons now perceive noxious input as coming from more than one source and a pain referral is experienced. muscle is more likely to be referred, and although the exact showed that this referral can cross to different spinal mechanism of this remains to be investigated, it is likely to cord levels in association with increased spinal cord levels relate to central (spinal) mechanisms. Mechanoreceptors in of substance P and CGRP. It is, therefore, theorised that the muscle have a lowered stimulation threshold in the presence increased release of substance P and CGRP in the dorsal of excitatory compounds such as bradykinin horn in response to a noxious stimulus diffuses around several levels of the spinal cord and increases the sensitivityof those areas to noxious input. The levels of these twotransmitters have been found to be independent, and it is not known if their source is local neurons or release from highercentres (). What was previously an Although, as previously stated, there is no evidence of innocuous stimulus may now be perceived as pain, and pain inflammation or increased levels of nociceptive transmitters may be perceived at a seemingly unrelated anatomical site.
in the region of trigger points, the most popular theories This may also apply to the newly opened receptive field, proposed to date assume that injury and mediator release is such that a pressure or tightness sensation in the muscle is the precipitant of trigger point related muscle pain, with these sensitised nociceptors then having increased responses Muscle spasm, as seen in many conditions of muscle pain to normal mechanical stimuli. Theories implicating a may relate to a connection between dorsal horn neurons in primary neurogenic cause do not share this weakness, the spinal cord and gamma afferent neurons. Gamma although lack any confirmatory data. Further clarification of afferent neurons supply muscle spindles and are responsible for reflex muscle shortening, such as that seen with tendon Once a painful stimulus is established, by whatever reflexes. Inhibition of dorsal horn neurons indirectly inhibits means, dorsal horn neurons may be sensitised and new receptive fields opened due to the flux of substance P andother transmitters at the spinal cord in response to the initialpain This neural plasticity may help to 10. Clinical precipitants for trigger point formation explain referred muscle pain and possibly be responsible forthe misinterpretation of signals previously recognised as Trigger points are thought to form in response to innocuous. Neural plasticity may be important in the increased or altered muscle demands. Muscle overload, as often seen in the pre-season conditioning phase of sport training, is one such example. Other mechanisms ofincreased or altered muscle demands include prolongedmuscle contraction, such as in workplace postural errors, proximal nerve compression and resultant muscle spasm,and post-trauma (). Latent trigger points The traditional theory used to explain the phenomenon of are thought to become activated in response to the same referred pain is the convergence projection theory. This conditions that cause trigger point formation, that is, muscle states that each dorsal horn neuron has connections from overload, prolonged muscle contraction, or nerve more than one body part. Noxious stimuli are only expected to arise in one of those body parts. When a noxious stimulus Trigger points can also be influenced by descending is received from another area, it is misinterpreted as coming factors such as stress or constitutional illnesses. The sympathetic ‘flight or fight’ response to stress is related to increases in the amount of circulating catecholamines. It has A modification of convergence projection theory postu- been shown that the EMG activity in trigger points can be lates that not all convergent connections are active all the reduced by the use of sympathetic antagonists time, but previously dormant spinal cord connections are and that it increases at times of stress ( unmasked in response to a painful stimulus ( L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 Trigger points should, therefore, be considered when assessing for the sources of pain in many different clinicalscenarios. For example, sedentary workers presenting with head or neck pain may exhibit thoracic spine tightness or Stretching after the application of a vapocoolant spray signs of early degenerative change in their cervical spine is reported by Travell and Simons (1983) to be the ‘single and may have a history of poor posture at work. They may most effective treatment’ for trigger point pain. An also have some elements of their pain reproduced with attempt was made to clarify this, using pain scales and palpation of trigger points in the trapezius, long neck pressure threshold as outcome measures for response to extensors, or sternocleidomastoid muscle. Similarly, a spray and stretch techniques in patients with chronic neck lumbar disc injury is often responsible for significant pain, but elements of this pain may be reproduced with pressure study used contralateral sides as controls in symptomatic on trigger points in the paraspinal, quadratus lumborum, or patients and was not blinded, it did show a significant gluteal muscles. Osteitis pubis may be accompanied by reduction in both reported pain and pain pressure trigger points in the adductor muscles or the gluteals.
threshold after the intervention. There was no correlation Importantly, trigger points can form in either of these between the improvements in these two parameters. It was regions purely in response to an increase in load, without postulated that the coolant spray acted by a counter- irritation mechanism. From these results, it is impossible Of interest, is that clinical syndromes seen may not to say if spray or stretch in isolation might have the same reflect the locality of the trigger points, but rather, their referral zones. Examples include posterior thigh pain reproduced from gluteal trigger points or achilles tendon program of ischaemic pressure and stretching to a program pain reproduced from calf trigger points. When assigning of stretching alone in subjects with trigger points in the causality for pain to trigger points, it is essential to assess trapezius region. Ischaemic pressure combined with stretch- carefully for the amount of contribution to the overall ing resulted in a greater improvement in pain scores and syndrome. To illustrate this, consider the following; the pain pressure threshold. The pressure was applied prior to commonest source of pain in the Achilles region is still the stretching and, therefore, could well have been acting in pathology at or around the Achilles tendon, but when this a counter-stimulatory fashion. Importantly, this research diagnosis is not clear cut on clinical assessment, trigger shows a benefit of massage techniques above the effect of points at a proximal location may enter into the therapist’s consideration. Likewise, when the pain complaint is out ofproportion to the evident local pathology, or when treatmentof a local area fails to completely relieve symptoms, if 11.1.2. Transcutaneous electrical nerve stimulation trigger points are a possible contributing factor, they should Transcutaneous electrical nerve stimulation (TENS) is be considered and carefully assessed. It is important not to often postulated for use in chronic pain and can be used at assign significance to trigger points if they do not produce different frequencies and intensities to attempt to achieve reproduction of a recognisable pain. Non-specific pain does not identify a contributing trigger point according to the 100 Hz, 2 Hz and control TENS on subjects with trigger point related chronic pain in the thoracic, neck, or head is one of the essential criteria for diagnosis of an active region. Low frequency and control TENS had no effect on pain, whereas the high frequency resulted in significantpain relief. None of the modalities resulted in any changein pain pressure threshold. postulated the results to be due to modulation of centralpain sensitivity. also found a reduction Trigger point therapy is essentially divided into invasive in pain with the use of 60 Hz TENS when compared to and non-invasive techniques. Non-invasive techniques are placebo, but interestingly also found a significantly greater those that have been traditionally employed by physical and improvement in pain threshold in the active group. A third manual therapists. In recent years, there has been marked arm of their trial used electrical muscle stimulation or increase in the use of invasive therapies, in particular, dry interferential. Although this group did not report the same needling to manage trigger points. Anecdotally, all therapies benefits on pain, they did exhibit a marked improvement in have their supporters. Scientifically, however, very few of range of cervical lateral flexion. Again, a central them stand up to scrutiny. Of those that do produce a result, mechanism of pain relief was postulated, but it was also a clear mechanism for this improvement has not been found, suggested that both modalities be tried together to but all share the feature of application of a noxious stimulus.
maximise effects on range of motion and pain. There is This section will describe the evidence for a variety of non- no data to date on the expected duration of any invasive and invasive methods of managing trigger points.
L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 letters to journals, however, and it wasn’t until much later A search of the literature only identified one well- that the therapies were more formally investigated. Most of designed trail on the use of ultrasound for the treatment of the substances listed are irritants to muscle and are not trigger points in patients with neck and shoulder myofascial considered in modern practice, however, local anaesthetics pain. Therapeutic ultrasound was used in a three-armed trial are still widely used. Interestingly, very early in the ultrasound with home exercise and massage, sham ultra- insertion of a needle somewhere in the region of the pain sound with home exercise and massage or a non-interven- without introducing analgesic solutions has been reported to tion control group. Both intervention groups showed give frequent lasting relief. This is the basis on which significant improvements in the number and sensitivity of investigation of dry needling began, and, to date, there is no trigger points, but the ultrasound had no additional evidence to convincingly refute his statement.
advantage. Despite the use of massage and stretching inthis trial, there was no reduction in pain scores or analgesic use in the subjects of any group. This contradicts the Local anaesthetic is certainly the substance most findings of the other studies on stretching discussed above, investigated for injection into trigger points. Many different agents have been used, and most of them have equivalentresults to the injection of normal saline Although some studies indicated potential benefits for finding is that the pain relief, when seen, well outlasts the expected half-life of the injected solution, suggesting mechanisms of pain relief above the pure pharmacological one of the anaesthetic. It must be noted, that in these studies it is extremely difficult to have a true placebo, particularly if double blinded trial on 18 patients with upper limb active Steinbrocker’s early comments are taken into account.
trigger points and found a significant reduction in pain Overall, local anaesthetic injection is most likely to threshold immediately, and a larger reduction at 15 min improve subjective outcome measures (e.g. pain scores) after therapy in the active laser group. used pulsed infrared laser in neck pain and found an improvement that was higher in the active group, but only at motion and pressure threshold have been reported day 24 after 12 treatments and after 3 months of follow up.
This may well be explained by central modulation of pain as the dominant factor in relief. This is supported by the conjunction with routine physiotherapy in a double blinded fact that in all of the above research reports pain relief far fashion. They found a significant increase in skin resistance outlasts the half-life of the local anaesthetics used, making it over trigger point sites with laser therapy that was unlikely to be a purely local phenomenon.
postulated to accompany the resolution of the pathology, Local anaesthetic use can result in reversible myotoxi- however, there is no data to date to corroborate this city, seen as ischaemia and necrosis of muscle fibres in the found no difference between five treatments of helium – These changes are much worse in the presence of neon laser and placebo on pain at any time point in a double vasoconstrictors (adrenaline). Perhaps this is simply the optimum form of counter-irritation, where a true inflamma- laser on neck and shoulder pain in a double blind trial, and tory response produces mediators sufficient to reset the found that subjective reports of improvement were higher in spinal transmission of pain, and hence, result in prolonged the placebo group. There is, therefore, no reproducible evidence to date of the benefit of using laser therapy in the Injection of the skin over the trigger point with sterile water has been postulated as an appropriate treatment ifcounter-stimulation is the active mechanism ( Although there was evidence for prolonged painrelief in long standing neck pain patients in the study of Literature exists from the first half of last century detailing the use of injection therapies for the treatment of number of injections at multiple points over three muscle pain, described as ‘fibrositis’. Most of these separate treatments. Sterile water injection (more painful) involved the injection of local anaesthetic formulations, resulted in greater improvements than saline injection but hypotonic glucose, urea, and quinine were also proposed (less painful). Subcutaneous injection is a very painful procedure that is generally not well tolerated by patients, and a large number of injections over multiple treatments muscle pain with injection were case reports, case series or are likely to influence patient compliance, despite L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 the existence of some evidence to say that it can reduce In a double blind randomised controlled trial, dry needling versus a non-penetrating placebo needling of the Of interest to those treating mainly acute or athletic pain gluteal muscles for trigger point related referred hamstring is that, injection therapy has been shown to have a more pain in athletes found no change in the chosen range of rapid onset of pain relief in those with isolated regional pain motion measures, but an equivalent improvement in activity than in those with multiple regions involved and longer related pain scores in both groups (Huguenin et al., A recent trial evaluated the use of acupuncture at distal points, local dry needling, and sham laser acupuncture on Botulinum toxin injection has been proposed for use in trigger point therapy, based on the assumption that there is Although none of the groups exhibited a large reduction excessive ACh release from motor nerve terminals.
in pain, it is interesting to note that the acupuncture group Botulinum toxin is produced by the bacteria Clostridium improved by 30%, whereas the other two groups did not. In botulinum and acts by blocking the release of ACh at the the dry needling protocol, the needle was moved within neuromuscular junction. Whilst one early pilot trial trigger points until a twitch response was seen. Twitch suggested a potential benefit over saline at 2 – 3 weeks responses are painful and do correlate with post-treatment soreness, and this may therefore have clouded the results research. In a double blind design of patients with unilateral seen. The most important point to be taken from this trial is neck pain, injection of saline or 50 or 100 units of botulinum the lack of response when a non-noxious placebo (sham toxin produced equivalent results. There was no dry needling or placebo groups. All three treatments resulted The major drawback to the use of dry needling over local in similarly improved pain scores and pain pressure anaesthetic injection is the higher incidence of post- treatment soreness (This would appear to be unexplained finding is that subsequent treatment of the maximal in the 24 h after therapy and is usually manageable non-responders from all groups (saline, 50 and 100 units with heat packs and stretching, but may be intolerable to Botox) with 100 units of Botox resulted in a significantly some patients, and therefore care with patient selection is better response in those who received 100 units of Botox as Dry needling involves multiple advances of an acupuncture-type needle into the muscle in the regionof a trigger point, aiming to reproduce the patient’s Given that dry needling appears to be as effective as local symptoms, visualise local twitch responses, and achieve anaesthetic, but has no convincing benefit over placebo relief of muscle tension and pain. Unfortunately, there treatment, the mechanism of action of all of these therapies are few well-designed published studies of this technique.
remains to be clarified. The placebo treatments used have In an early study, dry needling was found to be varied, but all have still involved the application of a equivalent to local anaesthetic, corticosteroid, and coolant penetrative or non-penetrative but nonetheless noxious spray in the treatment of lower back pain ( stimulus to the skin. Central opioid release is thought to produce a global reduction in pain perception by gating investigated subjects with tension headache and found spinal cord pain impulse transmission. This is known as that muscle dry needling resulted in equivalent improve- diffuse noxious inhibitory control. Reversal of local ments in pain and neck range of motion compared to anaesthetic-induced analgesia has been observed with the placebo (subcutaneous) dry needling. The methods of range of motion measurement in this study, however, This implicates the endogenous opioid system, which acts to produce hypoalgesia at a spinal cord level, to at least a In another study, a four armed blinded trial in dental partial extent in the reduction of pain seen with this therapy.
patients found no improvement in pain pressure threshold, This is the system implicated in the production of a runners’ but equivalent improvements in pain intensity and unplea- santness, regardless of group allocation ( important in production of the placebo effect ( ). Groups randomly received placebo needling, local anaesthetic plus placebo needling, dry needling plus placebo Beyond these suppositions, there is little hard evidence to local anaesthetic, or placebo dry needling plus placebo local date on the mechanisms of action of any of the therapies anaesthetic over two sessions. Interestingly, the placebo dry discussed. It is a notoriously hard area to research due to the needle used did penetrate to the subcutaneous, but not the interactions of so many systems on both a regional and whole-body level. Stress and the sympathetic nervous L.K. Huguenin / Physical Therapy in Sport 5 (2004) 2–12 system have been shown to increase pain perception, but the effect of these treatments on this system has not beenconclusively evaluated.
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