**2. Muscle pain produced by a needle during needle electromyography**

Meadows [1] studied muscle pain during needle electromyography. He stated that there are sensory receptors associated with skeletal muscle that may give rise to the sensation of pain as observed after ischaemic exercise, or injection of 5–6% sodium chloride. Another form of muscle pain is encountered during the insertion of a concentric EMG needle electrode. When an EMG needle electrode is inserted into a muscle, transient pain is usually experienced, but once the needle has come to rest, the subject may be unaware of its presence. Meadows studied needle pain with concentric needle electrodes with external diameter of 0.46 and 0.30 mm, respectively, on his own vastus medialis muscles. 'When the needle is slowly advanced through the skin, pain is experienced on piercing the skin and again on piercing the muscle fascia, the latter case having a duller and less well-localized character. Further advancing of the needle is then usually quite painless. However, on infrequent occasions, a variably painful point may be reached during such a steady advance. If the needle is further advanced the pain usually subsides but in a few instances was found to be so intense, that further insertion was not attempted. Occasionally when the needle was critically positioned the slightest pressure on its butt caused intense pain which ceased as soon as the pressure was discontinued. It was sometimes apparent, that the site of such pain spots coincided with an increased resistance to the advancing needle, similar to that felt on encountering the muscle fascia when first entering the muscle. In the region of end plate zone advancing the needle sometimes caused a stab of pain which was associated with a twitch of a small fascicle or sometimes a greater part of the muscle'. He also studied pain produced by electrical stimulation through a concentric needle electrode, with the tip of the needle, positioned immediately adjacent to an extremely painful spot in the muscle. Single pulse of 0.05 ms and <5 V produced delayed discomfort and 10/s stimulation produced severe pain. No visible contraction could be seen. The same stimulation in other areas of the muscle was quite painless. Thus it was concluded that there are 'pain spots' in muscle tissue. However, the histological nature of the receptors was obscure. One point was of interest: when a pain spot was encountered, it was sometimes found that there was an increased resistance to the advancement of the needle at this point, suggesting that the receptors may be associated with intramuscular fascial planes.

#### **3. Electromyography of pain spots, historical aspects**

The first description of spontaneous EMG activity in pain spots was given by Jasper and Ballem [2]. They found local action potentials comparable to those described by Snodgrass and Sperry [3], and observed that these potentials were associated with particularly acute pain [2]. They 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 the muscle spindle.

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.

Meadows [1] studied muscle pain during needle electromyography. He stated that there are sensory receptors associated with skeletal muscle that may give rise to the sensation of pain as observed after ischaemic exercise, or injection of 5–6% sodium chloride. Another form of muscle pain is encountered during the insertion of a concentric EMG needle electrode. When an EMG needle electrode is inserted into a muscle, transient pain is usually experienced, but once the needle has come to rest, the subject may be unaware of its presence. Meadows studied needle pain with concentric needle electrodes with external diameter of 0.46 and 0.30 mm, respectively, on his own vastus medialis muscles. 'When the needle is slowly advanced through the skin, pain is experienced on piercing the skin and again on piercing the muscle fascia, the latter case having a duller and less well-localized character. Further advancing of the needle is then usually quite painless. However, on infrequent occasions, a variably painful point may be reached during such a steady advance. If the needle is further advanced the pain usually subsides but in a few instances was found to be so intense, that further insertion was not attempted. Occasionally when the needle was critically positioned the slightest pressure on its butt caused intense pain which ceased as soon as the pressure was discontinued. It was sometimes apparent, that the site of such pain spots coincided with an increased resistance to the advancing needle, similar to that felt on encountering the muscle fascia when first entering the muscle. In the region of end plate zone advancing the needle sometimes caused a stab of pain which was associated with a twitch of a small fascicle or sometimes a greater part of the muscle'. He also studied pain produced by electrical stimulation through a concentric needle electrode, with the tip of the needle, positioned immediately adjacent to an extremely painful spot in the muscle. Single pulse of 0.05 ms and <5 V produced delayed discomfort and 10/s stimulation produced severe pain. No visible contraction could be seen. The same stimulation in other areas of the muscle was quite painless. Thus it was concluded that there are 'pain spots' in muscle tissue. However, the histological nature of the receptors was obscure. One point was of interest: when a pain spot was encountered, it was sometimes found that there was an increased resistance to the advancement of the needle at this

point, suggesting that the receptors may be associated with intramuscular fascial planes.

The first description of spontaneous EMG activity in pain spots was given by Jasper and Ballem [2]. They found local action potentials comparable to those described by Snodgrass and Sperry [3], and observed that these potentials were associated with particularly acute pain [2]. They

**3. Electromyography of pain spots, historical aspects**

**2. Muscle pain produced by a needle during needle** 

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

**electromyography**

#### **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 is partly due to a relatively high [K<sup>+</sup> ] in the fluid. This may contribute to the excitability of 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 IIIand 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 the primary and secondary endings to the length and changes in the length of the muscle [21]. Dynamic gamma neurons innervate the bag 1 fibre by a p2 plate ending. Static gamma neurons innervate the bag 2 fibre and chain fibres by the trail endings. Dynamic skeletofusimotor beta neurons innervate the bag 1 fibre and extrafusal slow oxidative type 1 muscle fibres by p1 plate endings. Static beta neurons innervate the long chain fibres and extrafusal fast oxidative type 2 muscle fibres by p1 plate endings [13]. Each spindle receives about 7 motor axons, mean 3.2 beta and 3.8 gamma axons. The bag 1 fibre is almost always separately innervated by dynamic beta and gamma axons. Static beta branches supply exclusively the long chain poles. The bag 2 and chain fibres may receive a completely or variously segregated input in each pole [13].

on another active spot, and even late responses resembling F-waves. Thus, muscle spindles are electrically active structures in EMG, working in a network of gamma and beta motor

In clinical EMG, EPSs may be confused with fibrillation potentials, which are spontaneous action potentials of muscle fibres, or pieces of muscle fibres, which have lost contact with their motor axons. The development of fibrillation potentials needs time and there may be both rhythmic and irregular fibrillation sequences [30]. However, fibrillation potentials are distinctly different from EPSs both by the wave form and by the firing properties [9]. There is also a rare type of fibrillation-like activity, 'myokymic' fibrillations, which are elicited by so-called 'giant miniature end plate potentials' [31, 32]. The essential difference between EPSs and fibrillation potentials is the fact that denervation causes prolongation of the refractory period of the muscle fibre and thus the fibrillation potential cannot recur as promptly as action potential in a normal muscle fibre [33]. This causes the relatively long minimum interpotential interval of both rhythmic and irregular fibrillation potentials [31]. On the contrary,

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 pain-

ful trigger points. Shah et al. [38] found significantly increased concentrations of [H<sup>+</sup>

frequencies that are 10–1000 times that of normal miniature end plate potentials [39].

kinin, 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

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

], brady-

Muscle Pain and Muscle Spindles

7

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

**6. End plate spikes are different from fibrillation potentials**

units and having specific reflex responses [27].

EPSs have numerous short intervals less than 30 ms [9].

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

## **5. Origin of end plate spikes**

Where is the origin of EPSs if they are not nerve potentials or postsynaptic muscle fibre action potentials, activated by peripheral nerve injury? Partanen and Nousiainen [22] suggested that EPSs are action potentials of intrafusal muscle fibres such as small nuclear bag and nuclear chain muscle fibres inside the muscle spindles. EPSs can also be observed in active sites after manoeuvres for activating the gamma and beta motor activity such as passive stretch of the muscle, voluntary effort and repetitive nerve stimulation [9]. If multichannel EMG recordings are used, there are also different propagation patterns of EPSs such as local junction potentials as those observed in nuclear bag fibres [23], propagation for a very short distance as in nuclear chain fibres and propagation like MUPS but with the EPS firing pattern, as in beta (skeletofusimotor) motor units [9, 24, 25]. EPSs were also conjectured to be confined to the end plate zone of a muscle [26]. In fact EPSs can be found far from the end plate zone [9, 27]. It is a misconception that MEPPs are observed solely at the end plate zone, where the extrafusal neuromuscular junctions are situated [26]. Actually, MEPPs which are found far from the end plate zone, are mostly intrafusal representing synaptic activity of motor p2, p1 and trail endings. These MEPPs are often associated with EPSs, that is, gamma and/or beta motor unit potentials. At the end plate zone, MEPPs representing an alpha motor nerve terminal are not associated with EPSs [27, 28]. However, there are also muscle spindles at the end plate zone and thus, also MEPPs with EPSs may be found there.

Each pole of the muscle spindle receives 4–5 different motor axons and each gamma or beta axon innervates several spindles, but in a selective manner [13]. Thus junction and action potentials arise in several different spindles, when gamma and beta motor units are activated. This can also be seen in multichannel needle EMG recording. Synchronously firing EPSs may be found in remote active sites of a muscle, if these sites are innervated with the same gamma motor unit [27]. If EPSs in different remote active sites of a muscle are not innervated by the same gamma motor units, EPS firing is asynchronous. Intramuscular EPSs are not seen in the surface EMG, but MUPs of surface EMG are seen in the intramuscular sites with EPSs [27]. EPSs cannot be activated voluntarily, but voluntarily stopping of this activity is possible [27, 29]. Active spots with EPSs can also be stimulated with the concentric needle electrode, using electric impulses. With such stimulation, a reflex response resembling a myotatic reflex can be recorded [27]. Stimulation of an active spot with very small electric stimuli yields a response on another active spot, and even late responses resembling F-waves. Thus, muscle spindles are electrically active structures in EMG, working in a network of gamma and beta motor units and having specific reflex responses [27].
