Myofascial trigger points: the current evidence

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Abstract

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, many fundamental questions remain unanswered. This paper aims to give the therapist a greater understanding of the current knowledge of mechanisms of muscle pain, treatments that have been shown to be effective, and the ways in which these treatments may produce their effect. Most effective treatments have at their core a form of counter-stimulation or application of a second noxious stimulus. It remains unclear if it is this counter-stimulation or more specific elements of muscle stimulation that are the active ingredients, but it is possible that each contributes to effective outcomes.

Introduction

Although myofascial trigger points are a widely recognised phenomenon in clinical practice, there remains much to be elucidated with regards to their pathophysiology, 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 fibromyalgia was based on anecdotal reports and the clinical experience of those using this form of treatment. Most popular beliefs are based on theories generated on this basis, and it is only in recent times that a more scientific approach to defining and treating the phenomenon of myofascial trigger points has developed. Despite this increasing interest, much of the fundamental understanding remains based in the theories of the early clinicians and still requires experimental verification.

Trigger points are most often discussed in the setting of myofascial pain syndromes, in which widespread or regional muscular pain is associated with hyperalgesia, psychological disturbance, and significant restriction of daily functioning (Harden et al., 2000). Most patients with these syndromes recall an inciting factor for their pain, however, some may not. Inciting factors may often seem quite trivial when assessed. It is not clear whether the psychological disturbance seen in these patients is a part of the pathology or merely reactive to the chronic pain state. Importantly, psychological disturbance, from whatever cause, will impact on a patient's interpretation of pain (Yunus et al., 1989) and, potentially, their response to treatment.

As trigger points can also occur in the absence of pain syndromes, this paper aims to address the current state of knowledge with respect to trigger points as an isolated phenomenon, rather than addressing treatment approaches to more generalised pain syndromes.

Trigger points can be seen in the setting of occupational or athletic injury due to muscle imbalances, postural deficiencies, or secondary to another underlying pathological process. Examples of the latter include trigger points in quadratus lumborum in association with an irritated lumbar disc, or gluteal trigger points in the presence of hip joint pathology. Desk workers may present with headaches that are reproducible with pressure over trapezius trigger points due to the prolonged muscle contraction in inappropriate postures, or the development of thoracic spine stiffness. It is important to assess for and treat any precipitating or perpetuating factors in the presence of trigger points in order to maximise the chance of a long-term response to any treatment approaches.

Early writings on trigger points and their treatment were sporadic and lacked uniformity of diagnostic criteria. The Trigger Point Manual (Simons et al., 1998, Travell and Simons, 1992) is the most popular and comprehensive reference for those involved in treating this condition. The theories of pathogenesis contained within this volume have subsequently been challenged, but never conclusively disproved and the definition of trigger points presented is still the most widely used in clinical practice.

Section snippets

Trigger points—definition

The classical and most commonly used description of trigger points is that by Simons et al., 1998, Travell and Simons, 1992. Travell and Simons define trigger points as the presence of exquisite tenderness at a nodule in a palpable taut band (of muscle). Trigger points are able to produce referred pain, either spontaneously or on digital compression. The clinical definition came to be that trigger points are localised areas of deep tenderness within a taut band of muscle. They exhibit a local

Examination findings

On palpation of a muscle, a trigger point is recognised as a local tender spot within a taut muscle band. If a trigger point is active, the patient will recognise the symptoms produced when pressure is applied to it. Latent trigger points will be painful on palpation, but the sensations will not be recognisable. A local twitch response has been described in response to ‘snapping palpation’ of the taut band, and to the introduction of a needle (Simons et al., 1998). Snapping palpation is

Pathology

Currently, there is no gold standard pathological test for the identification of trigger points. Therefore, much of the research into the pathophysiology of trigger points is directed towards indirectly verifying the common theories for their formation. Histological studies have been inconclusive, with either non-specific changes of fibrosis and absence of inflammatory cells, or negative findings (Yunus et al., 1986). Imaging of trigger points has not been shown to be reliable with thermography

Theories of pathogenesis

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 plausible explanation. There is a third, yet to be experimentally verified theory, which suggests the primary site of pathology to be the spinal nerve, with secondary muscle changes occurring (Gunn, 1997). The more widely accepted theory is centred on the muscle cell and motor endplate being the sites of primary pathology (Simons

EMG findings

A pattern of EMG activity said to be characteristic of trigger points was first described in human subjects by Hubbard and Berkhoff (1993) and subsequently investigated by several other researchers (Hong et al., 1995, McNulty et al., 1994, Simons et al., 1995). The pattern has been termed spontaneous electrical activity (SEA), and has subsequently also been confirmed in rabbit studies (Simons et al., 1995). SEA is seen as low amplitude background noise (50 μV), with superimposed high amplitude

Muscle pain

As early as 1938, the production of characteristic patterns of local and referred muscle pain was described in response to injection of hypertonic saline (Kellgren, 1938). Muscle pain is likely to be transmitted by Group III (A delta, thin myelinated) and Group IV (c, non myelinated) afferent nerve fibres, as for cutaneous pain (Franz and Mense, 1975, Simone et al., 1994). Neurotransmitters implicated in this pain response include bradykinin (Franz and Mense, 1975), serotonin (Ernberg et al.,

Trigger point pain

Although, as previously stated, there is no evidence of inflammation or increased levels of nociceptive transmitters in the region of trigger points, the most popular theories proposed to date assume that injury and mediator release is the precipitant of trigger point related muscle pain, with these sensitised nociceptors then having increased responses to normal mechanical stimuli. Theories implicating a primary neurogenic cause do not share this weakness, although lack any confirmatory data.

Pain referral from trigger points

The traditional theory used to explain the phenomenon of referred pain is the convergence projection theory. This states that each dorsal horn neuron has connections from more than one body part. Noxious stimuli are only expected to arise in one of those body parts. When a noxious stimulus is received from another area, it is misinterpreted as coming from the usual recognised site of pain (Gerwin, 1994, Mense, 1993).

A modification of convergence projection theory postulates that not all

Clinical precipitants for trigger point formation

Trigger points are thought to form in response to 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 of increased or altered muscle demands include prolonged muscle contraction, such as in workplace postural errors, proximal nerve compression and resultant muscle spasm, and post-trauma (Simons et al., 1998). Latent trigger points are thought to become activated in response to the same

Trigger point therapy

Trigger point therapy is essentially divided into invasive and non-invasive techniques. Non-invasive techniques are those that have been traditionally employed by physical and manual therapists. In recent years, there has been marked increase in the use of invasive therapies, in particular, dry needling to manage trigger points. Anecdotally, all therapies have their supporters. Scientifically, however, very few of them stand up to scrutiny. Of those that do produce a result, a clear mechanism

How do these treatments work?

Given that dry needling appears to be as effective as local anaesthetic, but has no convincing benefit over placebo treatment, the mechanism of action of all of these therapies remains to be clarified. The placebo treatments used have varied, but all have still involved the application of a penetrative or non-penetrative but nonetheless noxious stimulus to the skin. Central opioid release is thought to produce a global reduction in pain perception by gating spinal cord pain impulse

Conclusions

Although trigger point related pain is widely recognised by health professionals, reliable clinical evaluation and imaging for diagnosis still eludes us. Many treatments in widespread use are poorly validated and not necessarily more effective than placebo. The application of a noxious stimulus may be the key to obtaining improvements in pain perception. Less stimulatory interventions, such as laser and ultrasound, have not convincingly been shown to be beneficial. Most stimulatory

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