sarcomeres. The precise reasons for the formation or activation of a trigger point are not yet elucidated, but acute injury or chronic microtrauma to the muscle (e.g. sustained muscle contraction due to tension and poor posture) may disrupt the sarcoplasmic reticulum within the muscle cell. The local and referred pain is

caused by sensitisation of nociceptors in the immediate region of the endplates, which are associated with endplate noise.

Endplate noise is a characteristic of

trigger points and indicates abnormal endplate function. Endplate noise is from low-amplitude discharges (10–50 µV) in the taut band, whether the trigger points are painful or not. Intermittent high-amplitude discharges (up to 500 µV) are seen in painful trigger points (6). The electrical discharges have the characteristics of miniature endplate potentials except that they occur with a frequency that is 10 to 100 times greater than that of normal endplate potential discharges. They are likely to occur as the result of an abnormally excessive, spontaneous release of the neurotransmitter acetylcholine from the synaptic terminal of the motor nerve fibre (7). Simons (4) proposed that

excessive release of acetylcholine at the motor endplate produces taut bands in the affected muscle, which compress capillaries, thereby decreasing local blood flow and causing ischaemia.

Ischaemia limits the availability of

oxygen and glucose, thereby creating an “energy crisis” in the working muscle. As a result, potassium, histamine, substance P and other excitatory substances that activate peripheral nerve nociceptors are released, stimulating dorsal horn nociceptive neurons and causing pain. The shortened muscle bands are likely to stay in their shortened positions and this then creates a vicious cycle. A model for this vicious cycle is shown in Figure 2.

Although this hypothesis seems

attractive and convincing, the abnormally excessive spontaneous release of acetylcholine from the synaptic terminals of a motor nerve fibre has not been proved definitively. Endplate noise was found to be significantly related to trigger points in two independent studies (8,9) but

24

abnormal acetylcholine release (endplate noise)

increased muscle fiber tension (taut band)

DEFINITIONS

Sarcomere One of the segments into which a fibril of striated muscle is divided Nociceptor A sensory receptor that responds to pain Endplate potential The change in electrical potential of the muscle membrane caused by a neurotransmitter such as acetylcholine.

Concentrations of these substances were significantly greater in active trigger points than in latent trigger points and muscles that were free from trigger points. The findings support the hypothesis of the presence of local ischaemia and hypoxia, which is caused by regional shortening of sarcomeres (shortening requires high oxygen because of the continuous metabolic demand). The ischaemia results in elevated levels of sensitising substances in the active trigger points, accounting for local tenderness and referred pain.

release of sensitising

substances (pain)

Figure 2: Essential pathophysiological features in myofascial trigger points and their inter-relationship in the feedback cycle.

endplate noise is not generated by acetylcholine alone. If some other mechanism, such as an immune system reaction, were to block the normally prompt inactivation of acetylcholine within the synaptic cleft, the acetylcholine receptors in the post- junctional membrane would continue to produce noise from excessive numbers of miniature endplate potentials. Despite these concerns, there are three recent studies (10–12) that support the hypothesis of the release of excessive acetylcholine. A positive- feedback loop maintains these changes until the loop is interrupted. Two studies, by Shah et al. (10,11) used a single difficult technique to sample the histochemical milieu of trigger points. They had the same experimental protocol with different sample sizes. Both used a microdialysis system to show elevated levels of sensitising substances associated with pain and inflammation in active trigger points. Among them were protons (equivalent to inverse pH), bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor-µ, interleukin- 1µ, serotonin and norepinephrine.

The third study (12) used magnetic resonance elastography, an advancement of magnetic resonance imaging, to examine the phenomenon. The results showed that the taut bands had muscle stiffness of 9.0 <+/-> 0.9 kPa in one person with myofascial pain, which was not only above that of the surrounding musculature (6.2 <+/-> 0.8 kPa) but also above the 4.1 <+/-> 0.6 kPa value found in the control subject. The results from this study should be interpreted with caution as it was exploratory in nature and only involved two participants. Nevertheless, it provides further evidence to support the existence of taut muscle bands.

HOW IS MYOFASCIAL TRIGGER PAIN DIAGNOSED? In a clinical setting, physical examination and palpation is the only method of diagnosing pain (13). In 2002, Simons (6) outlined the diagnostic features of active myofascial points. These features are shown in Table 1.

TREATING MYOFASCIAL TRIGGER POINTS Myofascial points can be treated by injection therapy, manual therapy, surgery or acupuncture. Manual therapy will be discussed here, and for other treatment techniques readers are encouraged to visit the relevant literature.

As discussed earlier, these trigger points are caused by regional shortening of sarcomeres. The goals of

OR LIGAMENTS

TENDER KNOTS OR TAUT BANDS IN MUSCLES

sportEX dynamics 2010;26(Oct):23-27