Reframing myofascial pain syndrome: pathological disorder or adaptive protective response?

Abstract

Myofascial pain syndrome (MPS) is one of the most common causes of chronic pain. It is characterized by trigger points (TrPs) that are located within palpable taut bands (TBs) in muscles and their fascial structures. Traditionally, this clinical condition has been regarded as a dysfunction of the musculoskeletal system, commonly associated with mechanical overload, such as acute strain, repetitive movements, and/or abnormal posture holding. However, the intrinsic mechanisms underlying its development remain a subject of debate. This review proposes a paradigm shift: to consider MPS as a physiological protective response rather than a pathological disorder. From this perspective, the TrP–TB complex may represent a dual contributor to structural and functional protection. On the one hand, it might limit potentially harmful movements through local and segmental sensitization mechanisms. On the other hand, it could enhance joint stability by increasing the tension of the muscle fibers that form the TB and its intramuscular connective tissue, potentially augmenting proprioceptive input. This new perspective offers a revised conceptual framework in which phenomena traditionally interpreted as purposeless manifestations of painful dysfunction may instead be understood as defensive and/or compensatory responses. Such a perspective both broadens understanding of MPS and may encourage the development of treatment protocols that go beyond classical techniques, which focus mainly on inactivating TrPs and managing pain. This new perspective suggests incorporating strategies to modulate load, perform functional training, and address both peripheral and central sensitization within a comprehensive, multilevel framework. Ultimately, this perspective may help achieve more durable and sustainable therapeutic outcomes, possibly contributing to a reduction in the prevalence of pain-related disability associated with MPS.

Plain language summary

Is myofascial pain a disease—Or the body’s way of protecting its own musculoskeletal system?

Myofascial pain syndrome (MPS) is a common cause of long-lasting muscle pain. It involves sensitive areas called trigger points, found in taut bands of muscle and surrounding fascial tissue. These are associated with many chronic musculoskeletal conditions, including low back pain, neck pain, sciatica, shoulder pain, and others. Traditionally, MPS has been viewed as a form of damage or pathological injury within muscle fibres, caused by strain, poor posture, or repetitive movements. This review presents a new perspective. It suggests that MPS may not be a disorder, but rather the body’s way of protecting itself from further harm. Just as fever was once considered harmful but it is now widely recognised as a helpful physiological response to infection, MPS may also serve a protective function. Taut bands and trigger points may form in muscles to limit potentially harmful movements and improve joint stability by increasing muscle tension and body awareness—particularly in response to actual or potential damage to muscles and joints. The review offers a clear and well-supported possible explanation of the pathophysiological mechanisms behind this protective response, based on current medical evidence. It also recommends treatment approaches that go beyond simply relieving pain. These include exercises to improve movement, reduce mechanical strain, and enhance posture, along with interventions that help regulate how the nervous system processes and responds to pain. This broader strategy may lead to longer-lasting relief and help reduce disability caused by chronic muscle pain—both in individual patients and across the general population.

Keywords

musculoskeletal pain myofascial pain syndromes physiopathology rehabilitation trigger points

Introduction

Myofascial pain syndrome (MPS) is a regional condition characterized by painful trigger points (TrPs) within taut bands (TBs) in skeletal muscle. Because these structures are anatomically inseparable, we refer to them collectively as the TP–TB complex, which has been associated with both local and referred pain and may contribute to a restricted range of motion.^1,2 Historically, this condition has been known as chronic muscular rheumatism,³ fibrositis,⁴ myogelosis,⁵ and muscle hardening.⁶ The term myofascial pain was introduced by Travell and Rinzler in 1952,⁷ and was later established through the publications of Travell and Simons in 1983 and 1992.^8,9

MPS is among the most frequent causes of chronic musculoskeletal pain, with an estimated prevalence ranging from 20% to 93%.^10,11 Despite its clinical importance—particularly due to its association with conditions such as neck pain, low back pain, and other nonspecific chronic musculoskeletal disorders that lead to disability^12,13—its etiology and pathophysiology remain unclear. Classical models have not yet fully explained their origin or triggering factors.

The clinical presentation of MPS is well recognized in clinical practice. Clinicians frequently observe localized, hardened, and hypersensitive areas in muscles and their fascia that are often associated with a limited range of motion and poor response to conventional pharmacological treatments. The controversy lies in the underlying causes and mechanisms of MPS, not in its existence: What exactly are TrPs and TBs? Why do they form? What function might they serve in the musculoskeletal system?

Over the decades, various pathophysiological models have been proposed to address these questions, ranging from biochemical and inflammatory to neurogenic and metabolic theories. However, none has fully integrated the spectrum of clinical observations. In 2024, Zhai et al. called for fragmented models to be abandoned in favor of explanations that consider the interaction between external forces, motor control, and the neurophysiology of pain.¹⁴

The aim of this review is to propose a paradigm shift in which MPS is interpreted as a potentially reversible protective mechanism that may contribute to preserving the integrity of tissues as well as the function of joints (including their osseous, cartilaginous, capsular, and ligamentous components), muscles (with their fascia and tendons), and the nervous system that controls them. These components are collectively referred to as the osteo-myo-neuro-articular system (OMNAS).

From this perspective, activation of the TrP–TB complex may represent an adaptive response to mechanical overload (MO), which may limit movement and contribute to musculoskeletal stability. Within this model, compensatory physiological responses such as the TrP–TB complex may be initially interpreted as protective but could become potentially injurious when their resolution is not possible due to the coexistence of perpetuating factors.

The sections that follow first examine traditional theories that conceptualize MPS as a pathological entity, along with their limitations. Thereafter, the proposed reinterpretation—suggesting that MPS, rather than a disorder, may be conceived as a physiological adaptation to mechanical stress that could otherwise harm the OMNAS—is introduced.

Traditional approach: MPS as a pathological disorder

The integrated hypothesis by Simons

The most widely disseminated theory of MPS pathophysiology is the integrated hypothesis proposed by Simons et al.¹ This model proposes that an abnormal and sustained release of acetylcholine at the motor endplate induces persistent sarcomere contraction, forming so-called contraction knots. These focal contractures could compress adjacent blood vessels, leading to local ischemia, reduced ATP availability, and an energy crisis that promotes the release of algogenic substances. The resulting nociceptor sensitization may contribute to the formation of an active TrP and its associated TB, perpetuating a self-sustaining cycle of pain and dysfunction.

While this model has gained widespread acceptance, it presents several limitations. Notably, it does not adequately explain why the neuromuscular system would initiate such a response. Is it truly a dysfunction, or could it represent an organized reaction to a potentially harmful mechanical stimulus? In this regard, the integrated hypothesis—like other traditional models—focuses on the “how” of the phenomenon (biochemical mechanisms) but does not fully address the “why” (the functional significance of the response).

Some authors have questioned the histological demonstration of contraction knots and sustained acetylcholine release in human tissue. However, other studies have documented localized segmental sarcomeric contractions within myofascial TrP, both in human subjects and in experimental models.^15–17 The aim of this review is not to resolve the underlying basic science debate, but rather to reframe the interpretive lens: to consider whether these localized phenomena—regardless of their precise histological substrate—may be understood as components of a physiological response with compensatory and potentially protective value.

Travell and Simons identified a range of potential triggering factors for MPS, including trauma, overuse, poor posture, emotional stress, nutritional and metabolic disturbances, and chronic infections.^1,13 These systemic or contextual conditions may compromise the functional capacity of the OMNAS, rendering it more vulnerable to MO—even in low-demand scenarios. However, while these factors help explain systemic vulnerability, they do not fully account for the recurrent, localized, and anatomically specific manifestations of TrP–TB complexes. Nor do they explain why many patients, particularly sedentary individuals, develop TrPs in specific regions without any obvious mechanical stressors or identifiable acute overload. These clinical observations suggest that, beyond systemic contributors, regionally acting biomechanical and neurophysiological mechanisms are likely to play a role in the chronification and topographical recurrence of these syndromes. This reinforces the need for a model that integrates biomechanics, neurophysiology, and load regulation to explain the multifactorial nature of MPS.

Other theories on the pathological origin of MPS

Various alternative models have been proposed to address the shortcomings of Simons’ hypothesis, suggesting different pathophysiological mechanisms within skeletal muscle. Bron and Dommerholt, for example, attributed MPS to microtrauma in muscle tissue, which triggers the release of calcium ions into the cytoplasm.¹⁸ The Cinderella hypothesis suggests that, during prolonged contraction, the smallest motor units are disproportionately recruited, leading to metabolic overload, cellular damage, and impaired calcium regulation, all contributing to TrP formation.^19–21 However, within the physiological framework proposed in this review, sustained intracellular calcium elevation is interpreted as a secondary phenomenon that may be inherent to persistent neuromuscular activation, rather than as a primary pathological process.

Jafri suggested metabolic dysfunctions associated with reactive oxygen species.²² Fricton emphasized imbalances in cellular energy metabolism.²³ Stecco et al. implicated pathological changes in fascial tissue.²⁴ Partanen et al. highlighted dysfunction in the muscle spindle,²⁵ whereas Gerwin pointed to breakdowns in presynaptic and postsynaptic neuromuscular feedback mechanisms.²⁶ Despite their differences, the theories of these researchers share a common assumption: that the neuromuscular system might be failing in its physiological regulation, and that TrPs could represent a pathological manifestation of this dysfunction.

Some researchers have located the origin of TrPs outside the muscle. Quintner et al. proposed peripheral nerve dysfunction,²⁷ but Gunn suggested a radiculopathic process,²⁸ and Srbely emphasized mechanisms of central sensitization.²⁹ Although these perspectives offer new insights, they continue to frame MPS as a pathological event—a system error, dysfunction, or lesion. The possibility that TrPs and TBs could serve an adaptive, functional, or protective purpose has rarely been considered.

Limitations of the pathological models of MPS

The main limitations of these models are the lack of histological, neurochemical, or electromyographic confirmation, as well as their pathocentric lens. While they focus on explaining the how (biochemical or neurological mechanisms), they tend to neglect the why. This highlights the need for new interpretive frameworks. Current theories have not yet adequately explained the overlapping symptoms, variability in clinical expression, or progression toward more complex pain syndromes such as spinal segmental sensitization,³⁰ or fibromyalgia.³¹

Given these shortcomings, it is reasonable to ask whether MPS could instead represent a neurobiomechanical regulatory and alerting mechanism in response to a perceived threat to the musculoskeletal system. Within this framework, the formation of TrPs and TBs could be understood as a potentially protective and adaptive response that may contribute to preserving tissue integrity under conditions of MO. Together, these processes could constitute what is clinically recognized as MPS.

New proposal: MPS as a physiological response

This review proposes reinterpreting MPS as a physiological and potentially reversible protective mechanism that could help preserve tissue integrity and function within the OMNAS. From this perspective, the formation of a TrP–TB complex may be interpreted as an adaptive response to MO—one that may limit the range of motion and enhance joint stability. Three key concepts are essential to understanding this reinterpretation: MO, TrP sensitization, and the mechanical role of the TB.

MO has been suggested as the initiating factor. It is defined as any dynamic or static load that causes the adaptive capacity of the OMNAS to be exceeded.³² This may result either from (a) an external load that has excessive intensity, volume, or frequency or (b) a system with reduced adaptive capacity, that is, a dysfunctional OMNAS. In the first case, the load itself explains the MO. In the second, even low-demand activities, such as routine daily tasks, can cause MO and might elicit the formation of a TrP–TB complex.

Sensitization is the second factor, reinterpreted here as a protective strategy rather than as a pathology. A lowered nociceptive threshold and the presence of mechanical allodynia could create a state of functional restriction and protective rest, reducing the risk of further MO. Active TrPs, which produce spontaneous pain due to the accumulation of algogenic substances within a localized indurated nodule within a TB, may lead to motor inhibition and movement avoidance.^33,34 Latent TrPs, though silent in daily activity and only painful upon palpation, reflect a lower level of sensitization yet can act to limit exposure to potentially harmful mechanical stress. This interpretation aligns with other adaptive responses in the body. For example, fever syndrome was once viewed as pathological entity, but it is now widely recognized as a physiological protective mechanism regulated by the nervous system in response to noxious stimuli.³⁵

Finally, the third factor is the mechanical role of the TB, which consists of shortened extrafusal muscle fibers exhibiting increased passive tension, as supported by histological evidence of abnormally contracted sarcomeres in human myofascial TrP.¹⁶ Whether associated with active or latent TrPs, the TB may serve as a mechanical reinforcement for joint stability. In its active form, it can enhance allodynia through the tension it exerts, thereby restricting passive muscle elongation. In the latent form, it may help stabilize function by increasing tension in the connective tissue, thereby potentially improving proprioceptive input and motor control.

This integrative model proposes that the TrP, with its TB, forms a functional complex that is not merely an isolated pathological change but may represent a sequential adaptive response to MO. The manifestations of this complex vary based on the magnitude of the load and the functional state of the OMNAS. The following sections elaborate on specific hypotheses explaining the formation of the TrP–TB complex in both its active and latent forms, along with the physiological foundations that may support this proposal.

Active TrP–TB complex: Protective functional inhibition

In the proposed model, the active TrP–TB complex may be viewed as an adaptive response that could be produced by local, peripheral, and central nervous system mechanisms. The primary proposed role of the complex may be to reduce mobility and muscle activity in response to MO, in an attempt to prevent structural injury. Clinically, the active complex manifests through two main components: spontaneous and evoked pain, which may induce inhibition of reflexes and avoidance of movement; and the TB, which can increase passive resistance to stretch and further limit function. From this perspective, pain and mechanical allodynia are understood not as pathological manifestations but as protective signals that limit exposure to a perceived threat, in this case, MO.

Two types of mechanisms through which the TrP–TB complex is activated may be identified. The primary proposed mechanism is activation of the complex by high external loads—whether in intensity, volume, or frequency—such as trauma, explosive athletic movements, or repetitive tasks. The secondary mechanism occurs when low-intensity loads trigger activation only in the presence of a previously dysfunctional OMNAS, where the underlying dysfunction—not the applied load itself—is considered the primary contributing factor. The latter is commonly seen in sedentary individuals who are exposed to prolonged postural demands.³² In such cases, structures of the OMNAS undergo degeneration and progressive hypotrophy, rendering the system vulnerable to overload even during minimal activity. This may explain the onset of MPS during routine tasks.

The distinction between the two types of mechanisms may be clinically relevant because it influences treatment strategies. In a primary active TrP–TB complex, the first step is to reduce external load via training adjustments, ergonomic interventions, or workload control. In a secondary active TrP–TB complex, the priority is to restore system function through therapeutic exercise, motor control training, and reduction of sedentary behavior.

Figure 1 illustrates how dynamic MO of high magnitude—in terms of intensity, volume, or frequency—can threaten the tissue integrity of one or more OMNAS components. This activates a key TrP–TB complex, which may produce spontaneous pain via local sensitization, restricts movement, and induces functional inhibition. The resulting protective response can rely on movement avoidance behaviors to help prevent further or more severe MO.

Figure 1.

Model of the sequential activation of the primary active TrP-TB complex as a protective response to high-magnitude mechanical overload.

If an individual relies solely on analgesics without limiting the use of the affected segment, MO could lead to a persistent barrage of nociceptive input, potentially triggering a process of spinal segmental sensitization.^36–38 This may reflexively activate satellite TrPs in muscles innervated by the same segmental levels, amplifying pain and further reinforcing functional inhibition. The resulting relative rest may serve a protective role for the affected tissue by decreasing the likelihood of additional overload on the corresponding segment. Once the mechanical stressor is removed, the primary active TrP–TB complex (key and satellite) may evolve into a secondary latent TrP–TB complex or resolve completely.

In summary, the active TrP–TB complex can function as a nociceptive alarm system, potentially imposing functional rest proportional to the perceived risk. Its proposed role is to help prevent progression to tissue damage or minimize existing injury.

Latent TrP–TB complex: Stabilization and proprioceptive function

Unlike its active counterpart, the latent TrP–TB complex does not produce spontaneous pain or overtly inhibit function. Therefore, its physiological role appears oriented toward joint stabilization, not rest, through increased fascial tension. This increased tension may compensate for the loss of stiffness in the connective tissue that is induced by prolonged static postural loading, such as sitting or standing for prolonged periods. Such loading may cause chronic deformation of the fasciae, capsules, and ligaments comprising the OMNAS. This chronic deformation compromises the quality of proprioceptive signaling.

Experimental studies have shown that MO can cause mechanical uncoiling of the triple-helix structure in collagen fibers, resulting in damage at the molecular level without rupturing of the tissue, so-called subfailure. This correlates with altered tissue mechanics and leads to impaired motor control.^39,40

The mechanical integrity of connective tissue is relevant to the ability of mechanoreceptors to detect movement. Therefore, the molecular damage caused by MO disrupts their function, potentially undermining the stability of the OMNAS. Within this context, the primary latent TrP–TB complex is interpreted as an anticipatory strategy of the OMNAS to re-tension elongated tissue and improve motor control. This hypothesis may explain why latent TrPs are more commonly observed in the muscles that stabilize posture, such as the upper trapezius, gluteus medius, or quadratus lumborum.⁴¹

This state is not fixed. In response to a new dynamic MO, even of low intensity, the primary latent TrP–TB complex may convert to an active form, producing pain and restricting the range of motion. This mechanism could explain the onset of myofascial pain in sedentary individuals who, after prolonged static loading, experience pain while performing seemingly trivial movements, such as bending or reaching up.³⁴ In such cases, the term secondary active TrP–TB complex applies, as the complex becomes activated within an already dysfunctional system. Indeed, most cases of musculoskeletal pain without significant imaging findings (e.g., nonspecific low back or neck pain) may originate in this manner.

Furthermore, a secondary latent TrP–TB complex may be found that corresponds to the resting state of a previously active complex. This condition could explain the clinical recurrence of pain episodes in the same region, with palpable TrPs occurring even during asymptomatic periods. A study has described alterations in motor recruitment patterns associated with latent TrPs.⁴² While such findings have traditionally been interpreted as indicating a functional impact of the TrP itself, we propose the alternative hypothesis that neuromuscular dysfunction may precede and predispose the development of latent TrPs.

Figure 2 schematically illustrates how sustained postural static MO, such as prolonged sitting or standing due to work, study, or leisure, may lead to elongation of connective tissue, thereby degrading structural and functional integrity. This process impairs proprioceptive signaling, disrupting sensorimotor feedback and thus potentially contributing to motor control failure. As a compensatory response, the primary latent TrP–TB complex is activated, contributing to re-tensioning the system and partially restoring stabilizing capacity. This re-tensioning effect could help preserve proprioceptive integrity, mitigating the consequences of motor control dysfunction. In the state of compensated dysfunction, exposure to low-intensity, low-volume, or low-frequency loads may trigger the development of secondary active TrP–TB complexes, thereby potentially initiating all the pathophysiological events previously described for primary active complexes.

Figure 2.

Model of sequential formation of primary latent TrP–TB complex as an adaptive response to sustained postural stress and motor control dysfunction.

In clinical practice, however, it is common to encounter latent TrP–TB complexes in deep stabilizing muscles without any prior history of regional pain or restriction of motion. While stabilizing muscles are indeed more exposed to sustained mechanical loading—which may partly explain the high prevalence of TrP in these regions—the frequent observation of primary latent TrP–TB complexes in postural muscles, even in the absence of prior pain or functional limitation, suggests that their role may extend beyond a residual effect of overload. These cases may represent a distinct category—primary latent TrP–TB complexes—which emerge as adaptive responses from the outset, rather than as residuals of previously active states. Their proposed role is primarily proprioceptive and stabilising, particularly in postural muscles that support the spine and girdles.

A recent study reported an association between the presence of TrP and proprioceptive alterations in the neck.⁴³ Although the authors suggested that TrP may be the origin of these disturbances, we hypothesize that TrP may instead be the consequence. This perspective may help explain the findings in which alterations in position sense—affecting neck movement and posture—were less pronounced in latent TrP than in active TrP. While this mechanism may enhance neuromuscular control under static or repetitive stress, it also poses a therapeutic dilemma: deactivating these complexes might disrupt compensatory stability and provoke decompensation in vulnerable individuals. Although these hypotheses exceed the scope of the current manuscript, they raise important clinical questions for future investigations.

The distinction between these forms is more than academic: It may help define opposing therapeutic strategies. In individuals with a primary active TrP–TB complex, the priority would be to reduce external load. Conversely, in secondary presentations, the main intervention is to restore function through progressive exercise and postural control.

Neurophysiological basis of the TrP–TB complex as a protective response

To understand the pathophysiology of the TrP–TB complex, whether active or latent, the interactions among muscular, connective, and neural structures must be examined. Motor execution relies on integrating deep afferents such as kinaesthesia, pallaesthesia, and bathyaesthesia with their central nervous system processing to continuously adjust muscle tone and postural stability in real time.^44–49

When structural alterations such as sustained elongation of connective tissue or risk of injury to the OMNAS are detected, the central nervous system may activate reflex mechanisms to restore baseline tension and optimize afferent signaling. This could contribute to the formation of the TrP–TB complex. Capsuloligamentous mechanoreceptors are known to influence gamma-motoneuron activity via mono- and polysynaptic pathways,^50,51 increasing the sensitivity of muscle spindles and enhancing periarticular muscle tone.^52,53

Mechanical stimulation of ligaments and capsules can induce stabilizing reflexes without requiring nociceptive input,⁵⁴ which may help explain the silent behavior of muscles that harbor latent TrP–TB complexes. These reflexes have been documented as active stabilizing mechanisms in electromyographic studies,⁵⁵ and animal models have shown that gamma motoneurons are critical for maintaining coordination during postural shifts.⁵⁶

A characteristic finding in MPS is the localized twitch response elicited when TrPs are stimulated—a myotatic reflex that suggests the involvement of the muscle spindle and gamma and beta motoneurons in the genesis of the TrP–TB complex. Within this framework, the contribution of the muscle spindle to TrP formation is proposed as a physiological hypothesis, supported by indirect evidence from reflex physiology and sensorimotor control and animal models,^57,58 although direct experimental confirmation in MPS is still lacking. Moreover, the lesser-known beta motoneurons, which simultaneously innervate both intrafusal and extrafusal fibers,^59,60 may generate a sustained and localized contraction, as proposed by Partanen et al.,²⁵ expressed as a TB that could re-tension fascial tissue and potentially enhance proprioception without producing voluntary movement.

Neurogenic edema may also coexist within TB regions as a secondary phenomenon related to sustained mechanical stress and connective tissue sensitization, potentially contributing to hypoechoic ultrasound findings.²⁶ We propose that the rapid clinical reduction of the palpable TB after TrP deactivation may be a mechanically dependent process, in which resolving the active TrP component can lead to a decrease in passive connective tissue tension and partial restoration of motion.

Whereas gamma motoneurons modulate spindle sensitivity without generating contractile force, the spontaneous electrical activity recorded in TrPs originates mainly from extrafusal motor endplates.⁶¹ This is consistent with the hypothesis that both gamma and beta motoneurons reflexively contribute to the formation of the TrP–TB complex.²³

Finally, emotional and cognitive factors might also influence these mechanisms. Stress and aversive visual stimuli have been shown to increase the excitability of gamma motoneurons, enhancing spindle sensitivity.^62,63 Combined with dysfunction in the descending inhibitory pathways and sympathetic facilitation, this may partially explain the observed association between MPS and chronic emotional disorders.^64,65 Therefore, the TrP–TB complex does not respond exclusively to mechanical stress: once formed, it may be amplified by psycho-emotional triggers (Figure 3).⁶⁶

Figure 3.

Mechanisms involved in the formation of the TrP-TB complex as a protective response.

From this perspective, autonomic modulation—particularly sympathetic activation associated with psychological stress—may interact with the TrP–TB complex at multiple levels. Experimental evidence indicates that α-adrenergic blockades reduce high-frequency electromyographic activity within TrP, suggesting a possible facilitatory role of the sympathetic system in local neuromuscular excitability.⁶⁷

In addition, noradrenergic signaling can sensitize peripheral nociceptors, potentially amplifying active TrP pain,⁶⁸ while sustained stress responses—such as elevated cortisol levels and sleep disruption—may impair collagen turnover and tissue recovery.^69,70 Within our conceptual framework, these systemic influences are therefore viewed not as primary causes, but as modulators that may favor connective-tissue vulnerability and proprioceptive degradation (facilitating the emergence of primary latent TrP–TB complexes), as well as nociceptive sensitization (contributing to the persistence of active complexes). This integration remains a theoretical model that requires targeted experimental validation.

This proposed protective response mechanism aligns with the concept of increased allostatic load. This load—understood as the cumulative physiological or pathological burden generated by repeated or persistent stressors—drives multiple converging afferent inputs into the central nervous system.^71,72 The combined effect of these inputs may contribute to what is observed clinically as enhanced responsiveness across several neural and behavioral systems affecting the OMNAS. Importantly, this heightened reactivity may not be fully explained by central sensitization alone, but rather by the underlying allostatic load that gives rise to it.

Clinical and therapeutic implications

The purpose of this section is to illustrate how the newly proposed framework can help reorganize treatment strategies under a unified concept aligned with a structured pathophysiological sequence, rather than to analyze evidence for each therapeutic intervention for MPS. This conceptual structure for clinical diagnosis and subsequent therapeutic intervention is organized around three main events (Table 1).

Table 1.

Pathophysiological events, therapeutic objectives, and intervention strategies in myofascial pain syndrome.

Pathophysiological event	Primary therapeutic objectives	Recommended strategies
1. MO: (a) Excessive external loads in a functional OMNAS. (b) Normal external or internal loads in a reduced functional OMNAS.	Reduce or eliminate loads that exceed the adaptive capacity of the OMNAS: (a) Avoid trauma, reduce high-intensity efforts or activities at work or in sports practice. (b) Correct or compensate OMNAS deficiencies.	- Training adjustment (intensity, volume, frequency). - Optimization of rest and recovery. - Ergonomic education. - Active breaks. - Therapeutic exercise for strength, flexibility, and motor control. - Postural correction during occupational, recreational, and artistic activities. - Promote avoidance of sedentary behavior.
2. TrP–TB complex - Active - Latent	Restore mobility, reduce pain, and recover neuromuscular function	- TrP inactivation (manual therapy, dry needling, electrotherapy). - Mobility and stretching exercises. - Motor control training and strengthening. - Analgesic medication to facilitate adherence to therapeutic exercise.
3. Chronicity and Sensitization	Modulate nociceptive hyperexcitability and prevent disability	- Neuromodulatory medications (amitriptyline, duloxetine, pregabalin, tramadol). - Non-pharmacological techniques (physical modalities such as thermotherapy, electrotherapy, massage, acupuncture, dry or wet needling, etc.). - Psychological interventions.

The sequential and combined implementation of these strategies can be key to interrupting the progression toward central sensitization and achieving sustainable clinical outcomes.

MO, mechanical overload; OMNAS, osteo-myo-neuro-articular system; TB, taut band; TrP, trigger point.

Interventions to prevent or reduce MO

The initial event may arise from dynamic loading (e.g., sports, occupational activity, repetitive movements) or from sustained loading during static posture holding. The first therapeutic strategy may consist of identifying and reducing these contributing factors. In cases of dynamic MO, modifications include adapting training programs by reducing intensity, volume, and frequency; correcting technique; and optimizing rest and recovery periods.⁷³ For MO during static posture holding, recommended measures include obtaining ergonomic education, taking active breaks every 30–45 min, and adjusting posture in occupational, recreational, or artistic settings.⁷⁴

Strategies for deactivating and/or resolving the TrP–TB complex

The second event varies depending on the clinical presentation. In cases of active TrP–TB complexes, the goal is typically to deactivate the TrP and restore joint mobility. In cases of latent TrP–TB complexes, the aim is to restore motor control and joint stability through functional strengthening. In both scenarios, therapeutic exercise is generally considered the central tool, with substantial evidence supporting its role in improving function and reducing pain.⁷⁵ When both forms of the complex coexist, integrating strategies that target both symptom relief and functional correction is often necessary.

The use of analgesic medications may be beneficial for limited periods, with the goal of modulating nociception and improving adherence to therapeutic exercise programs.^36,76,77 This could be particularly helpful for individuals whose execution of movement is compromised by pain within the OMNAS.

Treatment of chronicity and sensitization

A lack of early intervention can facilitate the transition to peripheral and central sensitization, resulting in greater intensity and persistence of pain. At this stage, a multimodal approach becomes particularly important: Pharmacotherapy (such as amitriptyline, duloxetine, pregabalin, and tramadol), non-pharmacological analgesic techniques (such as electroanalgesia, e.g., transcutaneous electrical nerve stimulation—TENS), acupuncture, dry or wet needling, and manual therapy), and psychological interventions, combined with therapeutic exercise, have demonstrated effectiveness in several studies in moderating pain and improving function.^75,78–87

Depending on several clinical variables—including the location of TrP (predominantly stabilizing vs mobilizing muscles), the patient’s clinical history in relation to latent TrP (presence or absence of prior pain in the affected muscle), which allows differentiation between primary and secondary latent TrPs, functional physical examination findings (such as alterations in strength, motor control, and flexibility), exposure to dynamic loads (sports or occupational physical demands), sustained postural loading (sedentary work, poor ergonomics, physical inactivity), and psycho-emotional factors (anxiety, depression, sleep disturbances)—different phenotypes of patients with myofascial pain may emerge. These phenotypes may require differentiated therapeutic approaches that, in some cases, are even opposed.

For example, an active individual without significant psycho-emotional burden, presenting with primary active TrP in mobilizing muscles and exposed to excessive dynamic loads, may benefit primarily from TrP deactivation strategies combined with modulation of external MO. By contrast, a sedentary patient with anxiety and sleep disturbances, working in prolonged static postures and presenting with primary latent TrP in stabilizing muscles, may require a treatment strategy centered on ergonomic interventions, active breaks, motor retraining, regulation of sleep and emotional factors, and multimodal analgesia.

In summary, treating MPS should generally focus on deactivating TrPs as well as on addressing the underlying mechanisms that initiate the process, namely targeting MO, restoring motor control, and preventing chronicity. Within this framework, MPS may be interpreted not as a primary muscular dysfunction but rather as a physiological protective response to MO—one that could be reversible through sequential, targeted interventions guided by a rehabilitation specialist.

Limitations

As a narrative review proposing a reframing of existing hypotheses about MPS, the available high‑level evidence remains limited. Current literature provides insufficient reliable indicators to fully substantiate the proposed framework, and the exploratory nature of this work inherently restricts the depth of empirical support. These preliminary considerations reflect the early stage of development of this conceptual model, which proposes that the body may restrict motor activity and enhance joint support through evolved regulatory mechanisms expressed through MPS phenomena—particularly the TP–TB complex—in alignment with maintaining proper musculoskeletal function, and more specifically, the functionality of the OMNAS in states of MO.

This interpretation incorporates both teleonomical and, to some extent, teleological perspectives, which brings the discussion into broader philosophical considerations regarding function and adaptation in biological systems. While this may be viewed as a conceptual limitation, it also underscores areas where further clarification is needed and delineates a constructive direction for future research aimed at systematically testing, refining, and expanding the ideas presented.

This review incorporates several older references, reflecting our intention to revisit foundational concepts and accurately trace the historical evolution of the topic. While the age of some sources may be viewed as a limitation, these seminal works remain essential for contextualizing the development of the proposed ideas.

Conclusion

This review proposes a model in which MPS may be understood as a protective adaptive response to MO over the OMNAS. Viewed in this light, the adaptive effects described can be interpreted as expressions of functional plasticity and compensatory regulation, consistent with the teleonomic organization of biological systems. These mechanisms, however, can become potentially injurious over time when chronicity develops as a result of underlying drivers that are not adequately addressed.

Although contemporary management of MPS widely embraces a multimodal and holistic approach that includes ergonomic modifications, exercise, pharmacological treatment, physiotherapy, and invasive techniques, these strategies are often applied without a unifying pathophysiological framework that organizes them hierarchically according to their targets within the disease process. By linking therapeutic actions to specific stages of the proposed cascade—from MO to compensatory myofascial activation, to sensitization, pain, and functional impairment aimed at tissue protection—this approach may support more precise, integrative, and sustainable clinical decision-making.

From this perspective, a syndrome currently categorized as pathological or dysfunctional may warrant a more nuanced interpretation and could reframe its management, allowing therapeutic actions to be grouped and prioritized according to their mechanisms of action and their position within the pathophysiological sequence. This may help achieve more durable and sustainable therapeutic outcomes, contributing to a reduction in the prevalence of pain-related disability associated with MPS. Like any developing model, it requires validation through clinical, physiological, and biomechanical studies to determine its applicability, reproducibility, and potential impact on therapeutic practice.

Footnotes

Acknowledgements

The authors gratefully acknowledge Duilio Guzzardo, Mariano Blanche, and Virginia Gilli, members of EFID (Fundacion Equipo de Formacion e Investigacion en Dolor—Training and Research in Pain Team Foundation), Rosario, Argentina—for their valuable contributions to the conceptual framework discussed in several sections of this review. The authors acknowledge the professional editorial support provided by Editage, a division of Cactus Communications, in collaboration with SAGE Author Services. Editorial assistance included language and grammar refinement, as well as structural review of the manuscript. The authors confirm that the intellectual content and core ideas of the work were not modified during the editing process.

Declarations

ORCID iD

Tomas Nakazato-Nakamine

Use of artificial intelligence

In accordance with the journal’s policy, we disclose that generative AI tools were not used to produce scientific content, interpretations, or references. Their use was limited exclusively to minor language editing, such as grammar and clarity adjustments. All conceptual, analytical, and scientific contributions were developed, verified, and approved solely by the authors, who take full responsibility for the accuracy and integrity of the submitted manuscript.

References

Simons

Travell

Simons

. Travell & Simons’ myofascial pain and dysfunction: the trigger point manual. 2nd ed. Baltimore, MD: Williams & Wilkins, 1999.

Borg-Stein

Simons

. Myofascial pain. Arch Phys Med Rehabil 2002; 83(Suppl. 1): S40–S47.

Stockman

. The causes, pathology, and treatment of chronic rheumatism. Edinb Med J 1904; 15(3): 223–235.

Fletcher

. Fibrositis. Postgrad Med J 1937; 13(143): 324–329.

Schade

. Untersuchungen in der Erkältungstrade: III. Über den Rheumatismus, insbesondere den Muskelrheumatismus (Myogelose). Munch Med Wochenschr 1921; 68: 95–99.

Lange

. Muskelhärten und Hartspann. Dtsch Med Wochenschr 1933; 59(29): 1140–1141.

Travell

Rinzler

. The myofascial genesis of pain. Postgrad Med 1952; 11(5): 425–434.

Travell

Simons

. Myofascial pain and dysfunction: the trigger point manual. Vol. 1, the upper extremities. Baltimore, MD: Williams & Wilkins, 1983, 713 p.

Travell

Simons

. Myofascial pain and dysfunction: the trigger point manual. Vol. 2, the lower extremities. Baltimore, MD: Williams & Wilkins, 1992, 607 p.

10.

Urits

Charipova

Gress

, et al. Treatment and management of myofascial pain syndrome. Best Pract Res Clin Anaesthesiol 2020; 34(3): 427–448.

11.

Lam

Francio

Gustafson

, et al. Myofascial pain – a major player in musculoskeletal pain. Best Pract Res Clin Rheumatol 2024; 38(1): 101944.

12.

Barbero

Schneebeli

Koetsier

, et al. Myofascial pain syndrome and trigger points: evaluation and treatment in patients with musculoskeletal pain. Curr Opin Support Palliat Care 2019; 13(3): 270–276.

13.

Donnelly

Fernández-de-Las-Peñas

Finnegan

, et al. Travell, Simons & Simons’ myofascial pain and dysfunction: the trigger point manual. 3rd ed. Wolters Kluwer Health, Philadelphia, PA, 2018.

14.

Zhai

Jiang

Chen

, et al. Advancing musculoskeletal diagnosis and therapy: a comprehensive review of trigger point theory and muscle pain patterns. Front Med 2024; 11: 1433070.

15.

Gerwin

Cagnie

Petrovic

, et al. Foci of segmentally contracted sarcomeres in trapezius muscle biopsy specimens in myalgic and nonmyalgic human subjects: preliminary results. Pain Med 2020; 21(10): 2348–2356.

16.

Jin

Guo

Wang

, et al. The pathophysiological nature of sarcomeres in trigger points in patients with myofascial pain syndrome: a preliminary study. Eur J Pain 2020; 24(10): 1968–1978.

17.

Margalef

Sisquella

Bosque

, et al. Experimental myofascial trigger point creation in rodents. J Appl Physiol 2019; 126(1): 160–169.

18.

Bron

Dommerholt

. Etiology of myofascial trigger points. Curr Pain Headache Rep 2012; 16(5): 439–444.

19.

Kadefors

Forsman

Zoéga

, et al. Recruitment of low threshold motor-units in the trapezius muscle in different static arm positions. Ergonomics 1999; 42(2): 359–375.

20.

Hägg

. Human muscle fibre abnormalities related to occupational load. Eur J Appl Physiol 2000; 83(2): 159–165.

21.

Minerbi

Vulfsons

. Challenging the Cinderella hypothesis: a new model for the role of the motor unit recruitment pattern in the pathogenesis of myofascial pain syndrome in postural muscles. Rambam Maimonides Med J 2018; 9(3): e0021.

22.

Jafri

. Mechanisms of myofascial pain. Int Sch Res Not 2014; 2014: 523924.

23.

Fricton

. Myofascial pain: mechanisms to management. Oral Maxillofac Surg Clin N Am 2016; 28(3): 289–311.

24.

Stecco

Gesi

Stecco

, et al. Fascial components of the myofascial pain syndrome. Curr Pain Headache Rep 2013; 17(8): 352.

25.

Partanen

Ojala

Arokoski

JPA

. Myofascial syndrome and pain: a neurophysiological approach. Pathophysiology 2010; 17(1): 19–28.

26.

Gerwin

. A new unified theory of trigger point formation: failure of pre- and post-synaptic feedback control mechanisms. Int J Mol Sci 2023; 24(9): 8142.

27.

Quintner

Bove

Cohen

. A critical evaluation of the trigger point phenomenon. Rheumatology 2015; 54(3): 392–399.

28.

Gunn

. Radiculopathic pain: diagnosis and treatment of segmental irritation or sensitization. J Musculoskelet Pain 1997; 5(4): 119–134.

29.

Srbely

. New trends in the treatment and management of myofascial pain syndrome. Curr Pain Headache Rep 2010; 14(5): 346–352.

30.

Fischer

Imamura

Dubo

, et al. Spinal segmental sensitization. In: Braddom

(ed.) Physical medicine & rehabilitation secrets. 3rd ed. New York: Mosby, 2008, pp.610–625.

31.

Fernández-de-Las-Peñas

Arendt-Nielsen

. Myofascial pain and fibromyalgia: two different but overlapping disorders. Pain Manag 2016; 6(4): 401–408.

32.

Guzzardo

Arias-Vázquez

. The role of pre-nociceptive mechanical factors in the physiopathology of musculoskeletal pain. J Res Pract Musculoskelet Syst 2025; 9(1): 12–20.

33.

Shah

Thaker

Heimur

, et al. Myofascial trigger points then and now: a historical and scientific perspective. PM R 2015; 7(7): 746–761.

34.

Shah

Phillips

Danoff

, et al. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol 2005; 99(5): 1977–1984.

35.

Wrotek

LeGrand

Dzialuk

, et al. Let fever do its job. Evol Med Public Health 2021; 9(1): 26–35.

36.

Yap

. Myofascial pain—an overview. Ann Acad Med Singapore 2007; 36(1): 43–48.

37.

Nakazato

Romero

Guzzardo

. Spinal segmental sensitization as a common origin of chronic non-specific regional musculoskeletal pain: review of its pathophysiology and diagnosis. Phys Med Rehabil Res 2021; 6(1): 1–8.

38.

Nakazato-Nakamine

Romani

Gutierrez

, et al. Prevalence of spinal segmental sensitization syndrome in outpatients attending physical medicine and rehabilitation centers for chronic musculoskeletal pain: a multicenter study. Arch Phys Med Rehabil 2024; 105(9): 216–222.

39.

Zitnay

Weiss

. Load transfer, damage, and failure in ligaments and tendons. J Orthop Res 2018; 36(12): 3093–3104.

40.

Panjabi

. A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction. Eur Spine J 2006; 15(5): 668–676.

41.

Gerwin

. Classification, epidemiology, and natural history of myofascial pain syndrome. Curr Pain Headache Rep 2001; 5(5): 412–420.

42.

Lucas

Rich

Polus

. Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points. Clin Biomech 2010; 25(8): 765–770.

43.

Yılmaz

Kafa

Okan

. Does trigger point sensitivity affect proprioception? Effects of trigger point sensitivity in the upper trapezius muscle on proprioception. J Orthop Res Rehabil 2025; 3(3): 71–75.

44.

Riemann

Lephart

. The sensorimotor system, part I: the physiologic basis of functional joint stability. J Athl Train 2002; 37(1): 71–79.

45.

Riemann

Lephart

. The sensorimotor system, part II: the role of proprioception in motor control and functional joint stability. J Athl Train 2002; 37(1): 80–84.

46.

Cailliet

. The illustrated guide to functional anatomy of the musculoskeletal system. Chicago, IL: AMA Press, 2004.

47.

Clark

. Sensorimotor control of functional joint stability: scientific concepts, clinical considerations, and the articuloneuromuscular cascade paradigm in peripheral joint injury. Musculoskelet Sci Pract 2024; 74: 103198.

48.

Hunter

Brown

. Muscle: the primary stabilizer and mover of the skeletal system. In: Neumann

(ed.) Kinesiology of the musculoskeletal system: foundations for rehabilitation. 2nd ed. St. Louis, MO: Mosby, 2010. pp.47–75.

49.

Gutenbrunner

Lemoine

Yelnik

, et al. The field of competence of the specialist in physical and rehabilitation medicine (PRM). Ann Phys Rehabil Med 2011; 54(5): 298–318.

50.

Gardner

Johnson

. The somatosensory system: receptors and central pathways. In: Kandel

Schwartz

Jessell

, et al. (eds) Principles of neural science. 5th ed. New York: McGraw-Hill, 2012, pp.475–497.

51.

Sengupta

Bagnall

. Spinal interneurons: diversity and connectivity in motor control. Annu Rev Neurosci 2023; 46: 79–99.

52.

Mobargha

Rein

Hagert

. Ligamento-muscular reflex patterns following stimulation of a thumb carpometacarpal ligament: an electromyographic study. J Hand Surg Am 2019; 44(3): 248.e1–248.e9.

53.

Seitz

Murrmann

Ignatius

, et al. Neuromapping of the capsuloligamentous knee joint structures. Arthrosc Sports Med Rehabil 2021; 3(2): e555–e563.

54.

Johansson

Sjölander

Sojka

. Activity in receptor afferents from the anterior cruciate ligament evokes reflex effects on fusimotor neurones. Neurosci Res 1990; 8(1): 54–59.

55.

Schultz

Miller

Kerr

, et al. Mechanoreceptors in human cruciate ligaments: a histological study. J Bone Joint Surg Am 1984; 66(7): 1072–1076.

56.

Friese

Kaltschmidt

Ladle

, et al. Gamma and alpha motor neurons distinguished by expression of transcription factor Err3. Proc Natl Acad Sci U S A 2009; 106(32): 13588–13593.

57.

Partanen

. End plate spikes in the human electromyogram: revision of the fusimotor theory. J Physiol Paris 1999; 93(1–2): 155–166.

58.

Liu

Huang

, et al. The key role of muscle spindles in the pathogenesis of myofascial trigger points according to ramp-and-hold stretch and drug intervention in a rat model. Front Physiol 2024; 15: 1353407.

59.

Stifani

. Motor neurons and the generation of spinal motor neuron diversity. Front Cell Neurosci 2014; 8: 293.

60.

Manuel

Zytnicki

. Alpha, beta and gamma motoneurons: functional diversity in the motor system’s final pathway. J Integr Neurosci 2011; 10(3): 243–276.

61.

Fernández-de-las-Peñas

Yue

. Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med 2011; 6: 13.

62.

Onigata

Bunno

. Unpleasant visual stimuli increase the excitability of spinal motor neurons. Somatosens Mot Res 2020; 37(2): 59–62.

63.

Ribot-Ciscar

Ackerley

. Muscle proprioceptive feedback can be adapted to the behavioral and emotional context in humans. Curr Opin Physiol 2021; 20: 46–51.

64.

Schwarz

Yee

Mir

, et al. Noradrenaline triggers muscle tone by amplifying glutamate-driven excitation of somatic motoneurones in anaesthetized rats. J Physiol 2008; 586(23): 5787–5802.

65.

Lalchhuananwma

Sanghi

. The link between emotional and psychological distress with myofascial pain syndrome. Am J Sports Sci 2019; 7(4): 177–181.

66.

Koukoulithras

Plexousakis

Kolokotsios

, et al. A biopsychosocial model-based clinical approach in myofascial pain syndrome: a narrative review. Cureus 2021; 13(4): e14737.

67.

Hubbard

Berkoff

. Myofascial trigger points show spontaneous needle EMG activity. Spine 1993; 18(13): 1803–1807.

68.

Fernández-de-las-Peñas

Arendt-Nielsen

. Sympathetic facilitation of hyperalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain. Clin Neurophysiol 2006; 117(7): 1545–1550.

69.

Elenkov

Chrousos

. Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity. Ann N Y Acad Sci 2002; 966(1): 290–303.

70.

Dattilo

Antunes

HKM

Medeiros

, et al. Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis. Med Hypotheses 2011; 77(2): 220–222.

71.

Wallden

Nijs

. Before & beyond the pain: allostatic load, central sensitivity and their role in health and function. J Bodyw Mov Ther 2021; 27: 388–392.

72.

Sterling

. Allostasis: a model of predictive regulation. Physiol Behav 2012; 106(1): 5–15.

73.

Shariat

Cleland

Danaee

, et al. Effects of stretching exercise training and ergonomic modifications on musculoskeletal discomforts of office workers: a randomized controlled trial. Braz J Phys Ther 2018; 22(2): 144–153.

74.

Jensen

Finsen

Søgaard

, et al. Musculoskeletal symptoms and duration of computer and mouse use. Int J Ind Ergon 2002; 30(4): 265–276.

75.

Mata Diz

de Souza

JRLM

Leopoldino

AAO

, et al. Exercise, especially combined stretching and strengthening exercise, reduces myofascial pain: a systematic review. J Physiother 2017; 63(1): 17–22.

76.

Desai

Saini

. Myofascial pain syndrome: a treatment review. Pain Ther 2013; 2(1): 21–36.

77.

Vyvey

. Steroids as pain relief adjuvants. Can Fam Physician 2010; 56(12): 1295–1297.

78.

Bendtsen

Jensen

. Amitriptyline reduces myofascial tenderness in patients with chronic tension-type headache. Cephalalgia 2000; 20(6): 603–610.

79.

Zhou

Sun

, et al. Efficacy and safety of duloxetine in chronic musculoskeletal pain: a systematic review and meta-analysis. BMC Musculoskelet Disord 2023; 24(1): 394.

80.

Karamanlioglu

Geler Kulcu

Ozturk

, et al. Effectiveness of pregabalin treatment for trigger points in patients with comorbid myofascial pain syndrome and fibromyalgia syndrome: a randomized controlled trial. Somatosens Mot Res 2021; 38(4): 327–332.

81.

Schug

. The role of tramadol in current treatment strategies for musculoskeletal pain. Ther Clin Risk Manag 2007; 3(5): 717–723.

82.

Toopchizadeh

Izadseresht

Eftekharsadat

, et al. Effectiveness of transcutaneous electrical nerve stimulation (TENS) modality for treating myofascial pain syndrome: a systematic review and meta-analysis. J Res Clin Med 2024; 12(1): 14.

83.

Hong

. Myofascial pain therapy. J Musculoskelet Pain 2004; 12(3–4): 37–43.

84.

Fernández-de-Las-Peñas

Nijs

. Trigger point dry needling for the treatment of myofascial pain syndrome: current perspectives within a pain neuroscience paradigm. J Pain Res 2019; 12: 1899–1911.

85.

Bialosky

Bishop

Price

, et al. The mechanisms of manual therapy in the treatment of musculoskeletal pain: a comprehensive model. Man Ther 2009; 14(5): 531–538.

86.

Anwar

Zahid

Alexe

, et al. Effects of myofascial release technique along with cognitive behavior therapy in university students with chronic neck pain and forward head posture: a randomized clinical trial. Behav Sci 2024; 14(3): 205.

87.

Zhou

Liu

, et al. Is exercise rehabilitation an effective adjuvant to clinical treatment for myofascial trigger points? A systematic review and meta-analysis. J Pain Res 2023; 16: 245–256.