**Muscle Pain and Muscle Spindles Muscle Pain and Muscle Spindles**

#### Juhani V. Partanen Juhani V. Partanen Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

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

#### **Abstract**

Muscle pain is a common symptom associated with, for example, myofascial syndrome, fibromyalgia and polymyalgia rheumatica. Many diseases of the muscle tissue are, however, completely or nearly painless such as polymyositis and inclusion body myositis. Thus, a mere inflammation cannot be the cause of muscle pain. In needle electromyography (EMG), the insertion of a needle electrode causes pain but further advancement is usually painless. However, there are small spots of muscle tissue where sudden pain is elicited with the needle. In EMG, these 'active spots' are observed to produce spontaneous activity in the form of end plate noise and spikes (EPSs). End plate noise is elicited at the neuromuscular junction of α, β or γ motor neuron. EPSs are action potentials of γ or β motor units. Muscle spindles are the main nociceptors in muscle tissue, both in healthy muscle and in diseases with muscle pain by inflammation of the muscle spindles. Multiple possible mechanisms of muscle pain exist. Polymyalgia rheumatica may have interstitial pain and possibly pain associated with muscle spindle capsules. Delayed onset muscle soreness may reflect both interstitial muscle pain caused by minor injuries and pain generated in mildly inflamed muscle spindles.

DOI: 10.5772/intechopen.72223

**Keywords:** muscle pain, myalgia, myofascial syndrome, fibromyalgia, polymyalgia rheumatica, muscle spindle, nociception, fibrillation, fusimotor, electromyography, end plate activity, intrafusal, C-fibres, soreness, DOMS, trigger point, taut band, muscle afferents

#### **1. Introduction**

The generation of muscle pain is enigmatic. There may exist several mechanisms for pain production. Many diseases of the muscle tissue are completely or nearly painless, even if there are inflammatory histopathological findings. Thus, inflammation *per se* may not be reflected as muscle pain, although generally inflammation is considered to be associated with pain. In needle EMG, pain caused by the EMG needle seems to be localised in small spots. The EMG

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

activity in these 'active sites' consists of spontaneous electric activity (SEA), whereas in painless sites there is no spontaneous EMG activity. Trigger points, which are sensitive to manipulation and may be exquisitely painful, are a typical feature of muscle pain syndromes. Trigger points are situated in palpable taut bands of the muscle. The principal aim of this chapter is to discuss whether these localised pain spots may actually be inflamed muscle spindles with nociception.

conjectured that the needle tip was penetrating a nerve and called these potentials 'nerve potentials'. Kugelberg and Petersén [4] described similar potentials in clinical EMG as 'protracted irregular activity'. 'Such discharge was mostly irregular, might be ordinary motor unit potential as in fasciculation or little amplitude and duration as in fibrillation'. Jones et al. [5] further studied the origin of 'nerve potentials' with electrically injected iron marks at sites of their appearance and found most of these iron dots close to peripheral intramuscular nerve twigs. Buchthal and Rosenfalck [6] observed that miniature end plate potentials (MEPPs), or end plate noise, were often associated with this activity, which they called 'spontaneous diphasic spikes'. Finally, Brown and Varkey [7] proved that 'nerve potentials' were postsynaptic, recorded from muscle fibres. Thereafter, the term 'nerve potentials' was rejected and at present these potentials are called 'end plate spikes' (EPSs). The general consensus was that EPSs were activated by the EMG needle, which causes action potentials, when it touches an intramuscular nerve twig or nerve terminal. Action potentials are recorded postsynaptically with the EMG needle. It was not considered, that an ectopic nerve potential spreads to both directions from the site of its origin [8] and thus a motor unit potential (MUP) or fasciculation potential should be recorded, not an EPS [9]. In addition, experimental studies do not support the hypothesis that irregular sustained action potentials like EPSs be activated by peripheral nerve injury or irritation [10–12]. To discuss the origin of EPSs, we have to look at the physiological properties of

**4. Structure, vascular supply and innervation of the muscle spindle**

Human muscle spindles are 7–10 mm long fusiform fluid-filled capsulated organs with equatorial (A) and polar (B) regions. The capsule of the muscle spindle is a lamellated structure, which prevents the diffusion of extrafusal substances into the intrafusal periaxial space [13]. The mean thickness of the capsule is 1.8 μm in the B region, 4.2 μm in the juxta B and A and 7.6 μm in the A region [14]. The periaxial space is between the outer and inner capsule of the spindle and it is full of highly viscous gel. There is a transcapsular potential of −15 mV, which

the intrafusal endings. There are three types of intrafusal muscle fibres such as nuclear bag 1, nuclear bag 2 and nuclear chain fibres. One spindle has usually one bag 1 fibre, one bag 2 fibre and 4–7 nuclear chain fibres [13]. The muscle spindles are mainly distributed at the region of nerve entry into the muscle and around the subdivisions of the intramuscular nerves [13]. The distribution is thus different from that of the end plate zone, which usually is a relatively narrow band around muscle belly [15]. The main spindle artery is separated from those supplying extrafusal muscles, and in intrafusal capillaries, there is a blood nervous system barrier in both endoneurial and periaxial spaces [13]. The extrafusal capillaries are different and have efficient perfusion when compared to the intrafusal ones. Removal of substances which accumulate into the gel-filled periaxial space of the muscle spindle is a slow process. The sensory innervation of a muscle spindle consists of primary and secondary endings [13], and also III-

and IV-afferents [16–19]. Also, autonomic innervation has been observed [19, 20].

The motor innervation consists of fusimotor (gamma) and skeletofusimotor (beta) nerve axons, both of which also have dynamic and static components. They adjust the responses of

] in the fluid. This may contribute to the excitability of

Muscle Pain and Muscle Spindles

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

the muscle spindle.

is partly due to a relatively high [K<sup>+</sup>
