Introduction

A latent myofascial trigger point (MTP) is defined as a focus of hyperirritability in a muscle taut band that is clinically associated with local twitch response and tenderness and/or referred pain upon manual examination. Local tenderness and/or referred pain from a latent MTP are transient in duration upon mechanical stimulation, and a latent MTP exists without spontaneous pain [1, 2••]. A latent MTP can be verified objectively; for example, with intramuscular electromyography (EMG) showing spontaneous electrical activity (SEA) [3, 4] and/or ultrasound imaging technique showing a focal, hypoechoic region with reduced vibration amplitude [5]. Latent MTPs are prevalent in healthy patients and those with musculoskeletal pain, and may be a potential source of sensory-motor dysfunctions in humans. Though latent MTPs are not responsible for the spontaneous pain experience as the active MTPs are in patients, they may predispose the muscle to further damage and easily can be transformed into active MTPs under the influence of perpetuating factors in patients with chronic musculoskeletal pain conditions. This review highlights the potential mechanisms underlying those sensory-motor dysfunctions associated with latent MTPs and discusses the contribution of central sensitization associated with latent MTPs and the MTP network to the spatial propagation of pain and motor dysfunctions.

Mechanisms of Local Tenderness at Latent Myofascial Trigger Points

Extrafusal Motor Unit Hyperexcitability

Prolonged or unaccustomed exercise, low-load repetitive muscle work, acute and chronic mechanical and electrical trauma, sustained stress, and prolonged ischemia may lead to muscle cell damage and initiate the formation of the latent MTPs. The clinically evident progression from a nontender taut band to a tender taut band suggests that the first change in muscle is the development of the contracted, taut group of muscle fibers that can become painful when sufficiently stressed [2••]. Thus, a further understanding of the nature of motor unit hyperexcitability at latent MTPs may have important implications for the understanding of muscle pain and tenderness. An electrophysiological characteristic of an MTP is the existence of SEA registered with intramuscular EMG when the muscle is at rest [3, 4]. The SEA is a combination of endplate noise and endplate spikes. The endplate spike of several hundred–microvolt amplitude represents temporally summated miniature endplate potentials sufficient to reach or exceed the membrane threshold value [6, 7]. Hence, the spikes of the SEA represent postsynaptic muscle fiber action potentials from one or a few muscle fibers [8, 9]. These muscle fiber action potentials originate from extrafusal, but not intrafusal, motor endplates. It is known that it is not the contraction of intrafusal muscle fibers, but rather it is the contraction of extrafusal muscle fibers that contributes to the production of muscle force [10]. The motor unit behavior of the SEA is positively correlated with the force production during dynamic muscle contraction (Fig. 1). Thus, it is evident that the SEA indicates a state of sustained focal contraction and/or muscle cramps of extrafusal muscle fibers [2••, 11••]. Current evidence shows that motor unit hyperexcitability at latent MTPs plays a significant role in the induction of local tenderness and pain upon mechanical stimulation.

Fig. 1
figure 1

The linear correlation between wrist extension force and EMG activities from a latent myofascial trigger point in the extensor digitorum muscle. SEA is recorded with concentric-needle EMG electrode inserted into a latent myofascial trigger point; a pair of surface EMG electrodes is attached 2 cm distal to the needle EMG electrode. Note: there are also low-amplitude EMG activities in surface EMG following needle EMG insertion into a latent myofascial trigger point when the muscle is relaxed and without force output. EMG—electromyographic; SEA—spontaneous electrical activity

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Reciprocal Interaction between Motor Unit Hyperexcitability and Tenderness

Mechanical stimulation (such as manual palpation, dry needling, and acupuncture) of a latent MTP induces local pain and/or referred pain. An EMG needle insertion into a latent MTP in the forearm muscle induces local pain and/or referred pain. Local pain occurs immediately after EMG needle insertion into a latent MTP, and the induced local pain intensity positively associates with the amplitude and the duration of muscle cramp episodes [11••]. These results provide direct evidence that motor unit hyperexcitability can induce muscle pain. Direct evidence also exists to show that algesic substance glutamate injection into a latent MTP increases the occurrence rate of muscle cramps [12], and algesic substance hypertonic saline injection into the muscle decreases the frequency threshold for the development of electrically induced muscle cramps [13], indicating that muscle pain can increase motor unit excitability. Thus, there is a self-sustaining positive feedback loop between motor unit hyperexcitability and muscle pain associated with the MTP.

Motor unit dysfunction may have significant influence on the sensory characteristics of latent MTPs. Clinically, latent MTPs can be categorized into two types: local tenderness without referred pain and local tenderness with referred pain upon mechanical stimulation. The level of motor unit hyperexcitability may underline different clinical manifestations of latent MTPs upon mechanical stimulation. The occurrence of referred pain after EMG needle insertion into latent MTPs is positively associated with the duration and SEA amplitude of the muscle cramp episodes [11••], consistent with a previous result of a close relationship of local tenderness and motor unit excitability at MTPs [14]. Hence, sustained focal muscle fiber contraction only may be related to local tenderness without referred pain, and the development of focal muscle cramps may be the electrophysiological mechanism for local tenderness with referred pain upon mechanical stimulation of latent MTPs.

It is noteworthy that tenderness at latent MTPs is a localized event in the muscle; thus, peripheral mechanisms play a major role in the development of focal tenderness and pain. One of the potential peripheral mechanisms is that sustained focal muscle fiber contraction and/or muscle cramps at latent MTPs can induce focal ischemia or hypoxia, which has been explicitly documented by ultrasound imaging [5]. The contracting ischemic muscle fibers may release adenosine triphosphate (ATP), which may sensitize acid-sensing ion channel number 3 (ASIC3) by binding to P2X receptors. The ATP-induced sensitization of ASIC3 may render a sensory neuron more sensitive to ischemic acidosis, leading to the development of mechanical hyperalgesia and allodynia [15–17]. Mechanical compression to the muscle also has been reported to induce the release of ATP [18]. Thus, an increased level of ATP may be one of the major molecular mechanisms of local tenderness. Apart from the potential mechanisms of ATP in the muscle pain induction related to muscle ischemia, other algesic substances at active MTPs also may be involved at latent MTPs but in a lesser degree. These algesic substances include substance P, calcitonin gene-related peptide, bradykinin, serotonin, norepinephrine, glutamate, nerve growth factor, and cytokines [19, 20]. The effect of these algesic substances and the effect of sympathetic hyperactivity at MTPs are discussed in detail in a recent review [2••]. Muscle ergoreceptors of group III afferents, which are quite sensitive to light touch, also may be sensitized at latent MTPs and possibly contribute to local tenderness. However, this contention has not been explored.

In addition to nociceptor sensitization, non-nociceptors, which normally are not involved in pain, also are sensitized at latent MTPs and may contribute in a lesser degree to tenderness and pain induction [21]. Further, sustained muscle fiber contraction and/or muscle cramps may exert direct mechanical stimulation of nociceptors and induce tenderness [22]. The increased motor unit hyperexcitability and peripheral mechanical hyperalgesia may induce motor dysfunctions in healthy patients and in patients with musculoskeletal pain conditions.

Motor Dysfunctions Associated with Latent Myofascial Trigger Points

Accumulating evidence supports a close relationship between motor dysfunctions and latent MTPs. Current evidence shows that latent MTPs contribute to the development of muscle cramps, restricted joint range of motion (ROM), and muscle weakness and accelerated fatigability.

Muscle Cramps

Nocturnal calf-muscle cramps are common in both younger and older healthy patients. Neuromuscular hyperexcitability features, such as muscle cramps, fasciculations, and restless leg syndrome, also are commonly observed in patients with chronic musculoskeletal pain [23–25]. It now is evident that both active and latent MTPs are prevalent in patients with regional and generalized musculoskeletal pain. While active MTPs contribute to pain and motor dysfunction, latent MTPs may play a significant role in the neuromuscular hyperexcitability features in these patients. The increased motor unit hyperexcitability at latent MTPs constitutes one of the physiological mechanisms for the development of muscle cramps [11••, 12]. Alternative therapies (eg, manual therapy, acupuncture and/or dry needling, injection of Botulinum A toxin) targeted at latent MTPs may be a good alternative to the management of muscle cramps, fasciculations, and restless leg syndrome.

Restricted Joint Rage of Motion

Restricted joint ROM is commonly observed in healthy patients with latent MTPs. The number of latent MTPs has been reported to be negatively correlated with baseline ROM, and an improved knee-joint passive ROM is observed after nonpainful cross-fiber friction massage (MTP pressure release) over related latent MTPs [26]. MTP pressure release in the soleus muscle is effective on the restricted active ROM of ankle dorsiflexion [27]. Ultrasound therapy and ischemic pressure on the latent MTPs in the upper trapezius muscle increase the active ROM of the cervical spine [28]. Reduced muscle stiffness also has been found after thermal ultrasound therapy applied to the latent MTPs in the upper trapezius muscle [29]. This recent evidence further consolidates the concept that latent MTPs are one of the causes of the restricted ROM of a specific joint to the involved muscle [30]. The sympathetically maintained and sustained focal muscle fiber contraction [31] and/or muscle cramps [11••] within muscle taut band, and an increased afferent input from the muscle spindle to the extrafusal motor unit [32] at latent MTPs, may contribute to the shortened sarcomeres, inducing the shortening of the contracted taut band and, thus, the restricted joint ROM. Detailed mechanisms await further elucidation.

Muscle Weakness and Accelerated Fatigability

Prolonged dynamic exercise and sustained isometric contractions induce muscle fatigue, as manifested by decreased performance and a reduction in the maximum voluntary contraction force. It is a common clinical experience that a muscle harboring latent MTPs is weak and easily fatigued. However, the evidence on the muscle weakness and accelerated fatigability related to latent MTPs is sparse, though the decreased maximal voluntary contraction strength and accelerated fatigue are evident in patients with chronic musculoskeletal pain [33, 34]. The development of muscle fatigue is associated with increased EMG amplitude and decreased firing rate of the contributing motor units. Our preliminary result indicates that intramuscular EMG activity shows earlier occurrence of the reduction in the mean power spectral frequency from latent MTPs than that of normal muscle fibers during sustained isometric contraction until fatigue (Ge et al., unpublished data). This result suggests that latent MTPs are associated with accelerated muscle fatigability. The accelerated fatigability during muscle contraction may be related to a relatively low frequency of shifts between regions (differential activation) within a single muscle harboring latent MTPs. Motor unit hyperexcitability at latent MTPs may contribute to the sustained activation of taut muscle bands during muscle contraction. Using high-density surface EMG recording technique, a lower frequency of differential activation has been observed over the MTP regions compared to the normal muscle regions during computer work [35•], which is similar to the findings in the upper trapezius muscle of patients with fibromyalgia [36] (both latent and active MTPs are prevalent in this muscle [37]). Another potential mechanism is the existence of latent MTPs in a muscle inducing disordered muscle activation patterns in a group of functionally related muscles during a motor task, and the inefficient muscle recruitment possibly leading to muscle overuse and premature muscle fatigue [38•]. In addition to the changes in motor control mechanisms associated with MTPs, the contribution of structural and biochemical changes at latent MTPs to the muscle force production and fatigability still is unknown. Nonetheless, the accelerated fatigability associated with latent MTPs has adverse effect on movement control strategies because muscle fatigue induces increased spatial muscle activation within a single muscle [39] and an increased coactivation of agonist–antagonist muscle pairs [40], ensuing further damage to the muscle and muscle groups.

While evidence shows the contribution of latent MTPs to the development of muscle cramps, restricted joint ROM, and muscle weakness and accelerated fatigability, the role of latent MTPs in the disturbances of fine motor control, unstable force steadiness, and postural instability, among other dysfunctions, needs further evaluation, especially the contribution of muscle spindle afferents to disordered control of movement has not been explored.

In addition to the induction of local tenderness and motor dysfunctions, latent MTPs also exert a generalized effect on the sensory and motor systems.

Generalized Sensory and Motor Effect of Latent Myofascial Trigger Points

Central Sensitization Associated with Latent Myofascial Trigger Points

Mechanical stimulation (manual palpation and needle insertion) of latent MTPs with a higher sensitivity induces centrally mediated referred pain; thus, it is not surprising that latent MTPs have the potential to induce central sensitization. Apart from referred pain, which occurs a few seconds after mechanical stimulation of latent MTPs, a decreased mechanical pain threshold measured extrasegmentally also has been reported several minutes after nociceptive stimulation of a latent MTP in healthy patients [11••]. Referred pain from a latent MTP is dependent on its sensitivity and is short in duration. In contrast to the referred pain and spontaneous pain from an active MTP, which appears to reflect the formation of new effective central nervous connections, referred pain from a latent MTP is probably due to the fact that the latent MTP has only ineffective connections with the central nervous system and that these synapses are located on neurons that supply regions remote from the latent MTP [41]. The delayed onset of the decreased pressure pain threshold as compared to referred pain may reflect a temporary shift of dynamic balance of descending pain controls to net descending facilitation after tonic nociceptive stimulation of latent MTPs. However, when the central nervous system is in a sensitized state, such as in acute and chronic pain conditions, MTP sensitivity would be further increased [42•]. The clinical significance of these findings is that treating latent MTPs in patients with chronic musculoskeletal pain may not only decrease mechanical hyperalgesia and allodynia, but also prevent them from transforming into active MTPs.

Myofascial Trigger Points Network in Spatial Propagation of Pain and Motor Dysfunctions

In addition to the mutual influence of latent MTPs and central sensitization, more recent evidence points to the existence of MTP network, which may play a significant role in spatial propagation of pain and motor dysfunctions. Dry needling of a latent MTP in the extensor carpi radialis longus muscle has been reported to decrease the sensitivity of an active MTP in the upper trapezius and is associated with an improved pain and neck ROM [43•], and dry needling inactivation of an active MTP in the infraspinatus muscle can decrease the pressure pain sensitivity of a latent MTP in the extensor carpi radialis longus muscle [44]. Dry needling of an active MTP in the supraspinatus muscle decreases the mechanical pain sensitivity of another segmentally related active MTP [45]. Electrophysiological evidence further confirms the relationship between MTPs may be mediated by the changes of the SEA. It is reported that nociceptive chemical stimulation of a latent MTP in the infraspinatus muscle can increase the SEA of another latent MTP in the extensor carpi radialis brevis muscle and the variable onset time (a mean of 100s) for the increase in the SEA indicates that the response is not directly mediated via reflex pathways, but possibly via sympathetically mediated preferential activation of motor unit with lower motor activation threshold at MTPs [46•]. These results suggest that there are mutual interactions between MTPs at the segmental level in healthy patients and those with regional musculoskeletal pain. The mutual interactions also may exist in generalized musculoskeletal pain conditions. There also is evidence showing a decrease in overall spontaneous pain intensity and in pressure pain threshold at defined tender point sites after consecutive anaesthetic injections into a local active MTP in fibromyalgia [47], and these tender point sites specified by the American College of Rheumatology criteria are almost universally MTPs, either active or latent [48, 49]. Thus, mutual interactions exist between latent MTPs, between active and latent MTPs, and between active MTPs. It appears that proximally located MTPs have a stronger influence on distally located MTPs than the influence of the distally to proximally located MTPs, though further evaluation is warranted. Nonetheless, the MTP network may play an important role in the spatial propagation of pain and motor dysfunctions observed in chronic musculoskeletal pain conditions.

It also is important to note that when central sensitization already has established in chronic musculoskeletal pain conditions, such as fibromyalgia [37, 47] and osteoarthritis [50], the nociceptive drive from both latent and active MTPs may be enhanced by central sensitization, so latent and active MTPs in the whole MTP network may become more painful upon mechanical stimulation, corresponding to a higher occurrence of latent MTP with large referred pain area in fibromyalgia than healthy control patients [37]. The increased peripheral drive from these MTPs then may further enhance the central sensitization, and latent MTPs may be transformed easily into active MTPs under the influence of perpetuating factors. The latent MTPs, in addition to the active ones, should be integrated into the MTP management strategy.

Conclusions

The SEA originates from extrafusal motor endplate. The temporal profile of the SEA is similar to focal muscle fiber contraction and/or muscle cramp potentials. The motor unit hyperexcitability at latent MTPs contributes significantly to the induction of local tenderness and pain upon mechanical stimulation and to the local motor dysfunctions such as muscle cramps, restricted joint range of motion, and muscle weakness and accelerated fatigability. Central sensitization and the MTP network may have a significant effect on generalized sensory-motor dysfunctions in musculoskeletal pain conditions.