**7. Trigger points, taut bands and pain spots**

Muscle pain with trigger points (TrPs) is observed in myofascial syndrome and fibromyalgia. In fibromyalgia, there are also other pain spots outside the muscle tissue [34]. Myofascial syndrome is common in medical practice, but also latent TrPs are common in young, asymptomatic persons [35]. The main symptoms of myofascial syndrome are the presence of palpable taut bands in muscles, spot tenderness with TrPs, referred pain, pain recognition and twitch response [36]. The prevailing hypothesis for TrPs and taut bands in myofascial syndrome is 'the integrated trigger point hypothesis' [36, 37]. In short, muscle overload may cause local ischaemia and hypoxia with energy crisis. This causes increased acidity and acetyl choline leakage from the nerve terminal. This is seen as increased spontaneous electrical activity (SEA) in EMG and it achieves local sarcomere contraction knots in muscle fibres. These are felt as taut bands in the muscle. Ischaemia, energy crisis and contraction metabolites increase the local concentration of inflammatory and pain metabolites leading to the development of painful trigger points. Shah et al. [38] found significantly increased concentrations of [H<sup>+</sup> ], bradykinin, calcitonin gene-related peptide, substance P, tumour necrosis factor-α, interleukin-1β, serotonin and norepinephrine in active TrPs only. SEA in TrPs was stated to be different from spontaneous activity of normal neuromuscular junctions: the electrical discharges occur with frequencies that are 10–1000 times that of normal miniature end plate potentials [39].

However, in EMG studies, SEA is found in 5–10% of routine insertions of the needle into normal muscle [5, 40], without any evidence of dysfunctional end plates. The most common finding is EPSs with end plate noise in the background [25, 40]. For an electromyographer, it is very difficult to accept that MEPPs or end plate noise can achieve contraction knot in the postsynaptic area of the muscle fibre. These wave forms in EMG are a very common finding in quite normal muscles, without any taut bands or trigger points. The situation may be different in experimental studies, where the function of acetylcholinesterase was blocked [41]. The findings of microdialysis of trigger points [38] can be explained by intrafusal microdialysis: a twitch elicited by insertion of the capillary needle may show a myotatic reflex by the activation of intrafusal 1a-afferents of the given muscle spindle. Taut bands may be the final result of sustained reflex activation of beta motor units by intrafusal II-, III- and IV-afferents [25, 27, 28]. Trigger points comprise inflamed and painful muscle spindles with overactive nociceptive afferents. There are somatic thin nerve axons inside the muscle spindle and in its capsule [19]. Thus, it is also conceivable that pain spots in routine EMG of healthy muscles [1] are in fact muscle spindles. Extrafusal muscle fibres in rigour in taut bands cannot produce action potentials, but they can show end plate noise at the neuromuscular junction. Thus, the finding of Simons et al. [42] in myofascial pain can be explained: they found end plate noise (EPN) without spikes (EPSs) in TrPs of all 11 muscles studied, but EPN was found only at four sites at the end plate zone outside of TrPs. The spikes were also observed, but they occurred unexpectedly: one at TrP site, 12 at end plate zone outside TrPs and two at taut band sites. The plausible explanation is that spikes (action potentials of gamma or beta motor units) were mostly blocked in motor units in rigour in TrPs and taut bands, but were readily found outside of these sites [27]. Another issue is the occurrence of end plate activity inside and outside TrPs. Some studies reported end plate activity in every TrP and total absence of such activity in the control points [43, 44]. However, it was showed, that the difference between TrPs and control points, as to the number of EPSs, may even be non-significant [45]. The exception is the upper trapezius muscle, where EPSs are significantly more numerous in TrPs than in control points [45]. The latter explanation is consistent with the fact that there are inflamed muscle spindles (with EPSs) in TrPs and normal muscle spindles (with EPSs) at the control points [27].

points and taut bands are not typical for polymyalgia rheumatica, and muscle pain is evidently interstitial. EMG is usually normal, and this also is my experience as an electromyographist. Yet abnormalities consistent with either mild myopathic or neurogenic process have been reported in single patients [51]. There are numerous, but non-specific ultrastructural changes of muscle fibres in polymyalgia rheumatica. The endothelial cells of the capillaries showed no changes [52]. Any investigations on the histopathology of muscle spindles in polymyalgia rheumatica were not found. A tempting hypothesis is that there are inflammatory changes of the spindle capsule ('capsulitis'). The spindle capsule at about the equatorial region is made up of fibrous tissue lamellae which usually number 5–7, and are rather rich in endothelial-like nuclei. Among the lamellae lie several small blood vessels [53] as well as thin somatic nerve axons [18, 19]. The thick capsule on the equatorial area of the muscle spindle [14] may be felt as an increased resistance of the EMG needle resembling fascial planes [1, 27].

Muscle Pain and Muscle Spindles

9

http://dx.doi.org/10.5772/intechopen.72223

Eccentric muscle contractions cause lesions of the muscle membrane and also ultrastuctural damage of muscle fibres. These kinds of lesions are not observed after concentric muscle efforts [54]. Up to six hypothesised theories have been proposed for the mechanism of delayed onset muscle soreness (DOMS) after exercise: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. DOMS develops usually in 24 h after exercise in untrained persons [55]. It may be associated with fasciculations, visible spontaneous intermittent contractions of a portion of muscle. The origin of spontane-

We studied the appearance of muscle fasciculations after exercise with stretch-shortening cycle (SSC), with partly eccentric contractions. Nine healthy men, aged 25–50 years, were recruited for the study. Spontaneous fasciculations of the soleus muscle were recorded immediately before and at 11 min after 100 jumps with the ball of the right foot with extended knee joint. Fasciculation potentials were recorded with two concentric needle electrodes (diameter 0.3 mm), interelectrode distance 10 mm. The recording was performed before exercise, and 1–2, 4–5, 6–7 and 10–11 min after exercise with Dantec Keypoint EMG machine and Sony DAT recorder. The needles were removed temporarily, and were not used during the exercise. There was a significant increase of the number of fasciculations, beginning at 4–5 min after the 100 jumps and increasing thereafter (**Table 1**). Statistical analyses were performed using IBM SPSS Statistics for Windows (Version 24.0, IBM Corp., Armonk, NY). The differences between the number of fasciculations before and after the 100 jumps (i.e. 1–2, 4–5, 6–7 and 10–11 min after the jumps) were normally distributed, as assessed by the Shapiro-Wilk test (*p* > 0.05). Therefore, a paired-samples t-test was used to determine whether there was a statistically significant difference in the mean number of fasciculations before and after the 100 jumps; the test was repeated for the four conditions corresponding to 1–2, 4–5, 6–7 and 10–11 min after

**9. Delayed onset muscle soreness after exercise**

ous fasciculation potentials is mainly distal [56].

the jumps. The level of significance was set at *α* = 0.05.

**10. Fasciculations as a sign of muscle injury after exercise**

Ojala et al. [45] also found increased prevalence of complex repetitive discharges (CRDs) in 16% of patients with myofascial syndrome. CRDs may reflect ephaptic impulse transmission from II-afferents to gamma- or beta-motor efferents intrafusally. This may happen if the concentration of contraction metabolites, especially [K<sup>+</sup> ] is increased in the periaxial space of muscle spindles after sustained fusimotor activation [46].

## **8. Interstitial muscle pain**

Muscle pain is not always associated with trigger points and taut bands. Injection of hypertonic saline into the muscle causes pain [1, 47, 48], which evidently is interstitial activating mainly extrafusal pain C-fibres. C-fibres are known to be present in every tissue of the muscle with the exception of capillaries [18]. However, there is also evidence that hypertonic saline increases the sensitivity of muscle spindles to stretch [49], and thus also muscle spindles may be involved in the production of pain. The effect on pain caused by capsaicin injection does not differ from that of hypertonic saline injection [48]. In polymyalgia rheumatica, there is an abrupt onset of proximal pain and stiffness, especially in the neck and shoulder girdle. There are also signs of soft tissue oedema and inflammation. Tenosynovitis and bursitis are common. Polymyalgia rheumatica is also often associated with giant cell arteritis [50]. Trigger points and taut bands are not typical for polymyalgia rheumatica, and muscle pain is evidently interstitial. EMG is usually normal, and this also is my experience as an electromyographist. Yet abnormalities consistent with either mild myopathic or neurogenic process have been reported in single patients [51]. There are numerous, but non-specific ultrastructural changes of muscle fibres in polymyalgia rheumatica. The endothelial cells of the capillaries showed no changes [52]. Any investigations on the histopathology of muscle spindles in polymyalgia rheumatica were not found. A tempting hypothesis is that there are inflammatory changes of the spindle capsule ('capsulitis'). The spindle capsule at about the equatorial region is made up of fibrous tissue lamellae which usually number 5–7, and are rather rich in endothelial-like nuclei. Among the lamellae lie several small blood vessels [53] as well as thin somatic nerve axons [18, 19]. The thick capsule on the equatorial area of the muscle spindle [14] may be felt as an increased resistance of the EMG needle resembling fascial planes [1, 27].

## **9. Delayed onset muscle soreness after exercise**

postsynaptic area of the muscle fibre. These wave forms in EMG are a very common finding in quite normal muscles, without any taut bands or trigger points. The situation may be different in experimental studies, where the function of acetylcholinesterase was blocked [41]. The findings of microdialysis of trigger points [38] can be explained by intrafusal microdialysis: a twitch elicited by insertion of the capillary needle may show a myotatic reflex by the activation of intrafusal 1a-afferents of the given muscle spindle. Taut bands may be the final result of sustained reflex activation of beta motor units by intrafusal II-, III- and IV-afferents [25, 27, 28]. Trigger points comprise inflamed and painful muscle spindles with overactive nociceptive afferents. There are somatic thin nerve axons inside the muscle spindle and in its capsule [19]. Thus, it is also conceivable that pain spots in routine EMG of healthy muscles [1] are in fact muscle spindles. Extrafusal muscle fibres in rigour in taut bands cannot produce action potentials, but they can show end plate noise at the neuromuscular junction. Thus, the finding of Simons et al. [42] in myofascial pain can be explained: they found end plate noise (EPN) without spikes (EPSs) in TrPs of all 11 muscles studied, but EPN was found only at four sites at the end plate zone outside of TrPs. The spikes were also observed, but they occurred unexpectedly: one at TrP site, 12 at end plate zone outside TrPs and two at taut band sites. The plausible explanation is that spikes (action potentials of gamma or beta motor units) were mostly blocked in motor units in rigour in TrPs and taut bands, but were readily found outside of these sites [27]. Another issue is the occurrence of end plate activity inside and outside TrPs. Some studies reported end plate activity in every TrP and total absence of such activity in the control points [43, 44]. However, it was showed, that the difference between TrPs and control points, as to the number of EPSs, may even be non-significant [45]. The exception is the upper trapezius muscle, where EPSs are significantly more numerous in TrPs than in control points [45]. The latter explanation is consistent with the fact that there are inflamed muscle spindles (with EPSs) in TrPs and normal muscle spindles (with EPSs) at the control

8 Anatomy, Posture, Prevalence, Pain, Treatment and Interventions of Musculoskeletal Disorders

Ojala et al. [45] also found increased prevalence of complex repetitive discharges (CRDs) in 16% of patients with myofascial syndrome. CRDs may reflect ephaptic impulse transmission from II-afferents to gamma- or beta-motor efferents intrafusally. This may happen if the

Muscle pain is not always associated with trigger points and taut bands. Injection of hypertonic saline into the muscle causes pain [1, 47, 48], which evidently is interstitial activating mainly extrafusal pain C-fibres. C-fibres are known to be present in every tissue of the muscle with the exception of capillaries [18]. However, there is also evidence that hypertonic saline increases the sensitivity of muscle spindles to stretch [49], and thus also muscle spindles may be involved in the production of pain. The effect on pain caused by capsaicin injection does not differ from that of hypertonic saline injection [48]. In polymyalgia rheumatica, there is an abrupt onset of proximal pain and stiffness, especially in the neck and shoulder girdle. There are also signs of soft tissue oedema and inflammation. Tenosynovitis and bursitis are common. Polymyalgia rheumatica is also often associated with giant cell arteritis [50]. Trigger

] is increased in the periaxial space of

concentration of contraction metabolites, especially [K<sup>+</sup>

**8. Interstitial muscle pain**

muscle spindles after sustained fusimotor activation [46].

points [27].

Eccentric muscle contractions cause lesions of the muscle membrane and also ultrastuctural damage of muscle fibres. These kinds of lesions are not observed after concentric muscle efforts [54]. Up to six hypothesised theories have been proposed for the mechanism of delayed onset muscle soreness (DOMS) after exercise: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. DOMS develops usually in 24 h after exercise in untrained persons [55]. It may be associated with fasciculations, visible spontaneous intermittent contractions of a portion of muscle. The origin of spontaneous fasciculation potentials is mainly distal [56].
