Lecture Outline

Although myofascial pain is a common type of non-articular pain, its pathophysiology is only beginning to be understood due to its enormous complexity. Myofascial pain is characterized by the presence of myofascial trigger points, which are defined as hyperirritable nodules located within a taut band of skeletal muscle. Myofascial trigger points may be active (spontaneously painful and symptomatic) or latent (non-spontaneously painful). Painful myofascial trigger points activate muscle nociceptors that, upon sustained noxious stimulation, initiate peripheral and central sensitization.

Sensitisation is responsible for the transition from normal to aberrant pain perception—that is, when the central nervous system experience of pain outlasts the noxious stimulus coming from the periphery. There is a biochemical basis to the development of peripheral and central sensitisation in muscle pain. Continuous activation of muscle nociceptors leads to the co-release of substance P and glutamate at the pre-synaptic terminals of the dorsal horn and maximal opening of calcium-permeable ion channels. Moreover, prolonged noxious input may lead to long-term changes in gene expression, somatosensory processing and synaptic connections in the spinal cord and other higher structures. In addition, previously silent synapses may become effective. These mechanisms of sensitisation lower the activation threshold of afferent nerves and their central terminals, allowing them to fire even in response to daily innocuous stimuli. Consequently, even non-noxious stimuli such as light pressure and muscle movement can cause pain.

In order to investigate the peripheral factors that influence the sensitization process, we developed a microdialysis technique to quantitatively measure the biochemical milieu of skeletal muscle. Concentrations of bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor-α, interleukin-1β, serotonin, and norepinephrine were found to be significantly higher in subjects with an active trigger point compared to those with a latent one and those without trigger points in a standardized location in the upper trapezius muscle (p< 0.01). Furthermore, the concentration of specific biochemicals changes dramatically in response to initial needle insertion and also following a local twitch response, particularly in active MTrPs.

There are currently no imaging criteria for the diagnosis of myofascial trigger points or for assessing the clinical outcome of treatments. Therefore, it remains a clinical diagnosis based exclusively on history and physical examination. Accordingly, there is a need to develop objective, repeatable and reliable diagnostic tests for evaluating the nature and natural history of trigger points and determining treatment outcome measures. Our laboratory is using three types of ultrasound diagnostic imaging techniques—grayscale (2D Ultrasound), vibration sonoelastography, and Doppler—to differentiate tissue characteristics of trigger points in the upper trapezius muscle compared to surrounding soft tissue. We found that trigger points appeared as focal, hypoechoic regions on 2D ultrasound, indicating local changes in tissue echogenicity, and as focal regions of reduced vibration amplitude on vibration sonoelastography, indicating a localized area of stiffer tissue.

We have shown that ultrasound is feasible for imaging trigger points and that trigger points exhibit different echogenicity compared to surrounding muscle. Furthermore, vibration sonoelastography shows differences in relative stiffness between trigger points and normal (uninvolved) muscle. That is, sites containing trigger points have significantly greater relative stiffness compared to normal tissue. Doppler ultrasound was also able to show differences in the microcirculation in and around active trigger points compared to latent trigger points and normal tissue. For example, blood flow waveform characteristics can be used to differentiate active and latent trigger points. Retrograde flow on diastole was associated with active trigger points, indicating a very high resistance vascular bed and possible blood vessel compression.