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Muscle Fiber Dysfunction and Trigger Points — Brookbush Institute | Brentbrookbush.com

Muscle Fiber Dysfunction and Trigger Points

By Brent Brookbush, DPT, PT, COMT, MS, CES, PES, CSCS, H/FS, HMS


  • Trigger Point - "A hyper-irritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band. The spot is painful on compression and can give rise to characteristic referred pain, referred tenderness, motor dysfunction, and autonomic phenomena (1)."

There has been some debate regarding the "existence" of trigger points and whether they represent a phenomenon that should be addressed. The debate stems from treating the term "trigger point" as a structural entity, rather than a characteristic set of symptoms as described by the creators of the term. That is, the term "trigger point" is similar to the label "low back pain", and not "herniated nucleus pulposus (HNP)". The gross majority of opposing views on trigger points are based on a common fallacy:

Attack a term, based on the opposition's perceived definition of that term, rather than the expert's definition, published work and/or intent for using the label.

It is accurate to say that a characteristic set of symptoms exist, commonly referred to as a "trigger point“. There is a significant amount of evidence to demonstrate the prevalence of this characteristic set of symptoms, and further research to demonstrate the associated pathobiological changes to the motor unit. Insufficient technology has left some aspects of the pathobiological processes unexplained; however, insufficient technology leaves many questions unanswered, in every facet of sports medicine, especially those that involve cellular or molecular processes in living humans.

Some additional research may aid in defining trigger points. A series of studies by Vechiet et al. confirmed that trigger points resulted in a decrease in pain pressure threshold (more pain with less stimulus), and that pain was distinctly not cutaneous (7 - 10). Further, trigger points often exhibit characteristic referral pain patterns (1, 2, 4 - 7, 11-13), including burning and tingling that may mimic "nerve pain", pain in areas associated with other diseases, and may contribute to non-specific pain syndromes, such as low back pain, fibromyalgia syndrome (FS), and whiplash syndrome (11-15). Two reviews were located that provide evidence that acupuncture points and common trigger point sites are similar (16, 17). Last, although FS may be associated with trigger points, current research suggests that central sensitization is a key factor distinguishing FS from other types of myalgia (muscle pain). These studies refine our definition of trigger points by adding that they are acute points of increased sensitivity, that are not cutaneous, may result in referral pain patterns, may mimic other issues, may be similar to acupuncture sites, and are distinct from FS. 

Diagram of the "Integrated Trigger Point Hypothesis" from Dommerholt, J., Bron, C., & Franssen, J. (2006). Myofascial trigger points: an evidence-informed review. Journal of Manual & Manipulative Therapy, 14(4), 203-221.

Diagram of the "Integrated Trigger Point Hypothesis" - Dommerholt, J., Bron, C., & Franssen, J. (2006). Myofascial trigger points: an evidence-informed review. Journal of Manual & Manipulative Therapy, 14(4), 203-221.

Based on current research and the definition above, it is the assertion of the Brookbush Institute that more attention should be given to how terms related to the trigger point phenomena are "sorted." Although "sorting" and defining terms may seem like an esoteric activity, it has major implications for what terms mean, how they are used, and what research implies about them. For example, the term "trigger point" should be categorized in a continuum of clinically observable phenomenon that are the result of, or correlated with, the pathobiology of muscle fiber dysfunction. "Muscle fiber dysfunction," is a general term used to encompass all commonly noted changes resulting from excessive stress to a muscle fiber, and the clinically observable phenomena that result from those changes. Further the term "myalgia" should be viewed as a sub-category of clinically observable phenomena that result in the perception of pain. (Summary of terms below)

The term "myofascial pain syndrome (MPS)" is used in research (and in this paper when replacing the term MPS may misrepresent the findings of a study); however, it is the Brookbush Institute's opinion that this is similar to calling anterior shoulder pain, "shoulder impingement syndrome (SIS)". Rather than aiding in sorting a defined set of symptoms, it only aids in catastrophizing a common, non-specific set of symptoms related to orthopedic issues. Rather than labeling painful symptoms a syndrome, it is recommended that "myalgia" is a sufficient term for most muscle pain. Conversely, FS is appropriately termed a syndrome, as evidence of central sensitization implies a multi-faceted chronic condition, that must be addressed with an integrated approach to see any resolution of symptoms.

Last, although the term "muscle fiber dysfunction" has been chosen to describe the subject of this course, it is understood that this is a neuromyofascial phenomenon. The human movement system is undoubtedly holistic. However, labeling this phenomenon as "muscle fiber dysfunction" separates the subject matter from information that may explain dysfunction originating from damage to a joint (e.g. arthritis), damage to a nerve (e.g. neuropraxia) or damage to fascia (fasciitis).

Upper Body Trigger points: Posterior Deltoid, Upper Trapezius and Levator Scapulae

Upper Body Trigger points: Posterior Deltoid, Upper Trapezius and Levator Scapulae



  • Muscle fiber dysfunction - a general term used to encompass all commonly noted changes resulting from excessive stress to a muscle fiber, and the clinically observable phenomenon that result from those changes.
  • Myalgia - muscle pain, and/or the sub-category of clinically observable phenomena associated with muscle fiber dysfunction that include pain.
  • Trigger Point - "A hyper-irritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band. The spot is painful on compression and can give rise to characteristic referred pain, referred tenderness, motor dysfunction, and autonomic phenomena (1)."
  • Referred (Trigger Point) Pain - Pain that is generated by a trigger point, but is felt in a pattern that includes an area distal to that point. The pattern may be reproduced by stimulation of the original trigger point. Note, the distribution of referred trigger-point pain rarely completely congruent with the distribution of a peripheral nerve or dermatomal segment.
  • Tender Point/Latent Trigger Point - A myofascial trigger point that is not painful at rest, only painful when palpated, and may or may not exhibit a characteristic referral pain pattern when palpated.  Latent trigger points do result in an acute point of sensitivity, in a taut band of muscle, and may restrict range of motion (1).
  • Taut Band - an endogenous localized contracture within the muscle without activation of the motor endplate (2). Palpation can be used to highlight the difference in tissue tension between a taut band and the surrounding fibers, by slowly "strumming" a muscle perpendicular to the fiber direction. Taut bands are often described as feeling like a "guitar string wound too tight".
  • Twitch Response - A sudden contraction of fibers within a taut band when strummed (manually), needled, or compressed with a vibration massage device. The contractions may be observed visually, recorded electromyographically (EMG), or visualized with diagnostic ultrasound (3).
  • Myofascial Pain Syndrome (MPS) - Diagnosed pain syndrome that generally includes (4-7):
    1. Tenderness at points in firm bands of skeletal muscle
    2. Specific patterns of pain referral associated with each point
    3. Frequent emotional, postural, and behavioral contributing factors
    4. Frequent associated symptoms and concomitant diagnoses
    5. MPS is distinct from fibromyalgia
  • Fibromyalgia - A loosely defined diagnosis that is associated with widespread pain in combination with tenderness at 11 or more of the 18 specific tender point sites. Consideration may also be given to the presence of psychosocial stressors and inflammatory disease in the patients history. Newer research suggests that fibromyalgia may be at least in part due to central sensitization of myofascial pain, often associated with trigger points (261 - 271).

Below is an attempt to list observable phenomenon from least to most severe, or perhaps in association with least to most muscle fiber damage/maladaptation:

Observable Phenomena Associated with Muscle Fiber Dysfunction:

Based on clinical observations, many of these phenomenon may occur simultaneously. For example, pain on palpation is often associated with a general increase in tissue density and/or taut bands, with or without the presence of trigger points. Trigger points as defined above, likely represent a significant amount of muscle fiber dysfunction that includes maladaptation of the peripheral and central nervous system.

Pathobiology of Muscle Fiber Dysfunction:

  1. Excessive Stress
  2. Insufficient blood flow
    • Capillary restriction (especially during isometric contraction)
    • Insufficient recovery (cycling of motor units is insufficient)
  3. Metabolic crisis
    • Hypoxia
    • Cytochrome c-oxidase deficiency
    • Mitochondrial, sarcotubular system and cell membrane changes
    • Moth-eaten fibers and degeneration
  4. Muscle fiber changes
    • Taut bands and palpable nodules
    • Type I fiber hypertrophy
    • Increase in Type IIA fibers
    • Increase in transitional fibers
    • Preferential loss of Type I and/or Type II motor units
    • Infiltration of adipose and/or connective tissue
  5. Chemical change
    • Markers of inflammation and pain
    • Acidity (pH)
    • Excessive Ca2+
    • Excessive acetylcholine (ACh)
  6. Nervous system adaptation
    • Altered reflex sensitivity
    • Dorsal horn reorganization
    • Hippocampus inhibition
    • Autonomic system involvement
  7. Centralization

A significant amount of research correlates the pathobiology of muscle fiber dysfunction with clinically observable phenomenon. Although, it may be possible to highlight a lack of research to correlate a specific aspect of the pathobiology of muscle fiber dysfunction with a specific clinically observable phenomenon, when viewed in aggregate the relationship is well supported.

Special Note:

When referring to trigger points I am often challenged by individuals citing the following review:

I generally feel that publicly critiquing other credentialed professionals adds to the culture of "trolling", and with that in mind I try to refrain. However, there are certain claims in the industry that are being made, seemingly as part of a "contrarian movement", which are supported by little more than opinion, fallacies and the misrepresentation/interpretation of research. This paper falls into that category. The paper is full of biased language, false accusations, logical missteps, and academic dishonesty in the form of egregious errors in citation. This paper should not have been published, should be retracted, marks a poor job by the editorial staff of Rheumatology, and is a serious breach in professionalism by the authors and editors. Apologies should be demanded. You can read my notes on this review via the link below. Please keep in mind, these notes were not originally compiled with the intent of criticizing the authors; I was reviewing the article and its bibliography for continued work on the outline and annotated bibliography that developed into this article. Rather than the review adding wonderful alternative views, theories and citations, it proved to be a good example of how bias can destroy objectivity, and it stands as an example of how poor citation can destroy trust in the authors and potentially the journal. I also attempted to contact Rheumatology with my my notes in attempt to have the paper retracted, without ever making these notes public.  They did not respond.

Dr. Brookbush explains palpation and release of the flexor hallucis longus (FHL) and flexor digitorum longus (FDL) including common trigger point referral sites.

Flexor Hallucis Longus (FHL) and Flexor Digitorum Longus (FDL) Manual Release


General Prevalence

The presence of symptoms related to muscle fiber dysfunction, including trigger points, is undoubtedly common. In a Thai study of 2463 individuals, starting with a questionnaire and followed by clinician exam, 6.3% had symptoms matching myofascial pain syndrome (MPS) (18). A study by Fleckenstein et al. asked German physicians to estimate the number of patients diagnosed with MPS related pathologies in their clinics, resulting in an aggregate percentage of 46% ± 27.4% (19). A smaller study performed by internists practicing in Los Angeles reported 30% of office visits satisfied the criteria for MPS (20). Prevalence of jaw and face myofascial pain, over the course of a year, in a group of dental students was 19% (21), and a cross-sectional study on 171 randomly selected woman in a threshold country, reported 9% prevalence of jaw and face myofascial pain (22). A study by Han et al. demonstrated that every participant in the group of 4 - 11 year old children exhibited a decrease in pain pressure threshold (increased sensitivity) at a trigger point site in the brachioradialis, when compared to non-trigger point sites (23). This may suggest that the development of muscle fiber dysfunction and trigger points starts early and progresses over a lifetime. Research has also demonstrated that trigger points are more common in individuals who perform repetitive low-level muscle exertions as part of their daily activity, for example, office (desk/computer) workers, musicians, dentists, etc. (24 - 27). These numbers may not seem particularly impressive, but it should be considered that the findings in these studies are not the result of evaluating patients with known musculoskeletal complaints. The studies above are more representative of the prevalence of muscle fiber dysfunction in the larger population.

Joint Pain

The prevalence of trigger points and muscle fiber dysfunction increases substantially when trigger points are specifically assessed in individuals with musculoskeletal complaints (28 - 32). A study by Bajaj et al. demonstrated a significant increase in hip muscle trigger points in those with hip osteoarthritis (OA), an increase in knee muscle trigger points in those with knee OA, and a combined prevalence of 57% in OA patients (28). Studies by Bron et al., demonstrated that 100% of patients with shoulder pain exhibited trigger points, with the prevalence of active and latent trigger points varying between muscles of the shoulder and scapula (29). Fernandez-Carnero et al. demonstrated that active trigger points were found on the affected side, and latent trigger points found on the unaffected side, of all individuals in a group diagnosed with lateral epicondylitis (30). Weinner et al. demonstrated 96% prevalence of MPS symptoms in older adults with chronic non-specific low back pain (31). These studies seem to allude to a near ubiquitous development of muscle fiber dysfunction in conjunction with joint pain/pathology.

Cervical Pain, Headache and TMJ

Several studies have noted the prevalence of trigger points related to cervical pain, headache and temporomandibular joint syndrome (TMJ) (33 - 40). Studies by Cerezo-Téllez et al. and Muñoz-Muñoz et al. demonstrated an increase in active trigger points in those with mechanical and chronic neck pain, including 93.7% of patients exhibiting active trigger points in the upper trapezius (33, 34). A study by Sari et al. demonstrated both a difference in distribution and an increase in the number of active trigger points in those with cervical radiculopathy, as well as a significant proportion of asymptomatic individuals presenting with latent trigger points (for example, 40.2% of asymptomatic individuals had latent trigger points in the upper trapezius) (35). Studies by Fernánez-de-las-Peñas et al., Giamberardino et al. and Calandre et al. demonstrated a relationship between cervical trigger points and headaches/migraines (36 - 38)  Calandre et al. demonstrated that 93.9% of migraine sufferers exhibit active trigger points, with 74% found in temporal and/or suboccipital areas, and palpation of trigger points provoking migraine in 30.6% of patients. (36). Fernández-de-las-Peñas demonstrated that trigger points in the upper trapezius, sternocleidomastoid, and temporalis muscles were associated with chronic tension-type headaches, and that active trigger points were associated with greater headache intensity and longer duration when compared to the discovery of latent trigger points (37). Studies by Ardic et al. and Fernádenz-de-las-Peñas et al. demonstrate a relationship between TMJ and myofascial pain syndrome (MPS) (39, 40). Ardic et al. demonstrated 55 % of participants with TMJ had MPS symptoms (39). Fernádenz-de-las-Peñas et al. demonstrated referred pain from the neck contributed to TMJ symptoms, and that TMJ patients exhibited greater pain upon palpation in trigger point locations for the bilateral temporalis, deep masseter, superficial masseter, sternocleidomastoid, upper trapezius and suboccipital muscles (40). These studies suggest that the development of trigger points often accompanies head and neck issues.

Although further research is needed investigating additional musculoskeletal issues, the studies above imply that trigger points and muscle fiber dysfunction are very common, and strongly correlated with musculoskeletal pathology. The near ubiquitous discovery of trigger points in those exhibiting musculoskeletal issues may support an alternative hypothesis. That is, muscle fiber dysfunction and trigger points may be a component of all musculoskeletal pathology, representing a piece of an integrated model of dysfunction or compensation, that would also include known maladaptations such as, altered muscle recruitment, arthrokinematic stiffness/laxity, fascial dysfunction, inflammation and pain.

Excessive Stress

Trauma and Pain

There is general agreement among clinicians that acute musculoskeletal injury increases the prevalence and severity of symptoms related to muscle fiber dysfunction and trigger points. The prevalence of studies noted above, seem to imply that injury and trigger points are at least correlated (23 - 41). Unfortunately, most of these studies do not relate to acute injury. There is ample evidence (discussed below) of mechanical trauma causing direct injury to the cellular membrane, Ca2+ overload, and necrosis (166); however, these studies do not correlate damage with clinically observable signs. The strongest evidence to date investigating the relationship between trigger points and acute trauma are studies investigating the relationship between trigger point prevalence and whiplash syndrome (WS). Studies have demonstrated that early onset of acute hypersensitivity and an increase in the number of trigger points are prognostic indicators of recovery at 6 months (77 - 80). One study by Baker et al. reported the prevalence of trigger points in 50 WS patients was 77% in the splenius capitis, 62% in the semispinalis capitis, and 52% in the sternocleidomastoid (77). Two interesting studies by Fernández-de-las-Peñas et al. demonstrated the treatment of muscle fiber dysfunction (manipulation and trigger point therapy) was more effective for WPS patients than conventional therapy (active exercises, electrotherapy, ultrasound therapy and diathermy) (81, 82). Additional research has demonstrated the effectiveness of exercise for cervical dysfunction (83 - 87), which may suggest the aggregate of these studies should be interpreted as manual therapy more effective than modalities. Last, a study by Gunn et al. demonstrated that patients diagnosed with low-back strain and no tender points were disabled for an average of 6.9 weeks, while those with tender points were disabled for an average of 19.7 weeks (89). Although more research is needed investigating the correlation between clinically observable signs (e.g. trigger points) and acute muscle fiber damage, there is sufficient evidence to consider the relationship. More research is also needed on the sequential pathobiological events that follow acute trauma to aid in understanding pathobiological mechanisms, correlated symptoms and optimal treatment.

Continuous low-load activity:

The development of non-acute muscle fiber dysfunction is thought to be a result of tissue over-load, often resulting from near continuous low-load activity without sufficient recovery. Several theories have been proposed to explain the chronic development of trigger points and muscle fiber dysfunction, including the "Energy-crisis", the "Cinderella Hypothesis" (supported by Henneman's size principle (46 - 51)), the "Shift Model", and the "Brussel's Model". (1, 42 - 46). These models are not mutually exclusive, may coexist, and are generally in agreement regarding a set of over-arching "stages". These stages would include: excessive stress results in insufficient blood flow, creating an energy crisis, resulting in cell damage, resulting in the release of chemicals and neurotransmitters that may stimulate receptors associated with clinically observable signs (e.g. pain).

Several studies have demonstrated a decrease in blood flow (ischemia) within a muscle during contraction, which is especially pronounced during long-duration isometric contractions (52 - 56). This may include reliance on similar motor units during repetitive tasks, which may represent a "local" isometric contraction that could disrupt optimal blood flow for specific motor units. Studies have demonstrated either a reliance on a small number of motor units, a reliance on similar motor units with one or more continuously active motor units, a tendency of symptomatic individuals to rely on fewer motor units than asymptomatic individuals, and/or relative hypoxia associated with continuous low-load, long duration tasks (49 - 56). The reliance on similar motor units is a central tenant of the "Cinderella Hypothesis"; a hypothesis named for motor units that are recruited first and still "working" after other units are no longer active (46). Some studies have challenged the "Cinderella Hypothesis" with evidence of the "cycling" of motor units during long-duration activity, proposing that insufficient rest between periods of activity is a more accurate description of how fibers are overloaded (43, 62-66). Although this is likely an important detail for modeling physiological processes, it likely has little impact on assessment and interventions for muscle fiber dysfunction. That is, whether continuous activation or insufficient rest between cycles results in hypoxia does not matter to the clinician, as commonly used interventions likely address the resulting dysfunction and are not specific enough to address cycling versus isometric occlusion.

Several features of muscle architecture and motor control may contribute to the reliance on a small group of low-threshold, type I fibers for low-load activity. First, low-threshold motor units seem to have different control features (69), almost as if adapted for use during continuous low-load activity to the exclusion of larger motor units. Considering "Henneman's size principle," these control features may be related to Henneman's observation that smaller units are recruited first (46 - 51). It is likely that tissue architecture also contributes. Most type I fibers extend the entire distance from proximal to distal end, have relatively constant cross-sectional areas, and terminate in blunt ending, while type II fibers terminate between fascicles at one end, and the cross‐sectional area decreases progressively along its length (71, 72). This arrangement would imply that type I fibers are the first "tensioned" during any contraction or length change, as type II fibers would have to rely on a collective increase in tension of the connective tissue architecture of a muscle for the transmission of force. Research supports this notion, demonstrating that type I fibers are more resistant to stretch, stretch tension develops faster in type I fibers, and type I fibers demonstrate shortening at the ends while lengthening at the middle during eccentric contraction (73 - 76). Inter-muscular force generation is more random when maximal volitional isometric contraction (MVIC) is less than 20% (60). This may be due in-part to a phenomenon observed in a study on frog muscles, demonstrating longitudinal force generated by a muscle was equal to lateral force generation (77). Further research is needed to determine the effect lateral force generation has on the connective tissue architecture, and how stiffness of the connective tissue architecture would increase lateral force transmission to attachments. However, it may be hypothesized that the relatively random force generation at low-loads is partly the result of a loss of force to adjacent in-active (not stiff) fibers, reducing efficiency and resulting in greater strain on low-threshold motor units relative to the force needed for the task. The "Cinderella Hypothesis" and reliance on low-threshold, Type I fibers, may be due in large part to inherent control features and characteristics of tissue architecture.

The development of non-acute muscle fiber dysfunction and characteristic symptoms is common, which may have contributed to the amount of research and number of working models regarding this phenomenon. The research to date suggests that motor control, muscle architecture and blood flow play key roles in the development of muscle fiber dysfunction resulting from continuous low-load activity. The correlation between non-acute muscle fiber dysfunction and chronic injuries should be investigated further.


Many clinicians, texts and researchers have referred to a relationship between trigger point development and posture or postural dysfunction. The near ubiquitous presence of trigger points in those with musculoskeletal pathology may be considered evidence of a likely relationship; however, more direct evidence exists. Understanding the impact of constant low-load activity may provide a mechanism of tissue injury, as changes in posture often result in small increases in tissue stress that are persistent. Two studies that provide direct evidence of a relationship between posture and trigger point development - Hoyle et al. demonstrated trigger points developed in just an hour of continuous typing in a "high postural stress position (slouching)" (91), and Fernández-de-las-Peñas demonstrated that an increased number of trigger points was associated with forward head posture and chronic tension-type headaches (92).

Several studies demonstrate changes in stress and motion associated with trigger points that may exacerbate muscle fiber dysfunction. Lucas et al. demonstrated that latent trigger points were associated with altered scapular motion during arm elevation (94, 95). Ge et al. demonstrated latent trigger points increased fatigability of the upper trapezius during an isometric contraction (96). Note, these studies also demonstrated that treatment reversed these trends (94 - 96). Maher et al. demonstrated that sitting increased the shear stress modulus on trigger points when compared to lying in prone (93). This may be evidence that tissues are sheared and pulled around the hyper-contracted region of a trigger point within a muscle. These findings are not only evidence that trigger points may result in changes to reinforce further development, they are also similar to those described by studies correlating postural dysfunction with changes in scapular motion (103 - 106). (See Upper Body Dysfunction (UBD) for more information)

Three studies discussed below, also imply that the temporal and spatial summation of pain can result in a fairly rapid increases in sensitivity and dorsal horn re-organization (within a few hours) (262, 263). That is, pain intensity and sensitization is amplified by the proximity to the original site, rate of the stimuli and whether the area was already painful. This may allude to a mechanism of pain development in those exhibiting postural dysfunction, as changes in posture are often constant, persistent, and progress over time. Sjøgaard et al. provides a great review of the relationship between mental load, computer work, altered motor control patterns, altered motor unit activity, myalgia and muscle cell damage (97). These cascades may provide a framework that can be used to investigate the relationship between posture, muscle fiber dysfunction and pain at other body segments (e.g. Lower Extremity Dysfunction (LED)).

As altered muscle lengths are a tenant of postural dysfunction models, it is worth mentioning here that there is a relationship between length change/stretch reflex and muscle fiber dysfunction. A series of animal studies demonstrates that stretch, via mechanical tension on integrins, may result in the mechanical release of neurotransmitters and CA2+ (98 - 100). This may alter the activity/excitability of a muscle cell, and/or it may have deleterious effects on the muscle cell via the cascade associated with excessive CA2+ (discussed below). Several studies have also demonstrated a relationship between trigger points and altered stretch reflex. Mense et al. describes a relationship between norepinephrine (NE) and depressed feedback control of muscle length (101), and Shwartz et al. demonstrates this may increase tone by amplifying glutamate driven excitation (102). Note, several studies have demonstrated an increase in NE associated with active trigger points (see below). Ge et al. provides more direct evidence of this relationship, demonstrating that trigger points exhibit higher H-reflex (electrically induced stretch reflex) amplitude and lower H-reflex threshold, than non-MTrPs respectively, suggesting that muscle spindle afferents may be involved (230).

The correlation (and perhaps causation) between postural dysfunction and musculoskeletal pain/injury has been well established (see postural dysfunction/movement impairment). Posture is a source of constant low-load activity, which provides a mechanism for trigger point development. Trigger points have been correlated with changes in motion, fatigability, and control of stretch reflex (length/activity), which appear similar to changes noted in those exhibiting postural dysfunction. Further research is needed to investigate the relationships between postural dysfunction, muscle fiber dysfunction and trigger points.

Eccentric Loading

Several studies have noted that eccentric loading results in structural changes, chemical changes, altered capacity to generate force and pain (107 - 110), similar to those associated with muscle fiber dysfunction. The study by Nie et al. provides specific evidence of a link between eccentric loading, muscle fiber damage and clinically observable signs; demonstrating a relationship between eccentric loading, delayed onset muscle soreness (DOMS) and pressure induced pain (100). Further a study by Itoh et al., noted a decrease in pain pressure threshold and the development of taut bands seven days post eccentric exercise (123). Structural changes after eccentric exercise include cytoskeletal disruptions, Z-disk streaming, A-band disorganization, and hyper-contracted regions (101, 102). These hyper-contracted regions, may be similar to those noted by Mense et al.; hypothesized to be the physical phenomenon resulting in the palpable nodules associated with trigger points (198). The protein "desmin" may be particularly important to sarcomere structure, muscle fiber dysfunction and recovery (103 - 106). Research has demonstrated that one of the earliest measurable events post eccentric exercise (within 15 minutes) is a loss of immunostaining for desmin (103 - 104). This results in a tremendous amount of disorganization of contractile filaments (115). Further, a sharp increase in desmin-to-actin ratio over the following 72-hours has been noted, which may signal recovery (116). If this disorganization is related to hyper-contracted regions and palpable nodules, the role of desmin in active and latent trigger points may be an interesting area of study. Further consideration may be given to eccentric exercise and the decrease in strength, endurance, fine-motor skills, and increase in peak angle with and without pain (108, 116-118), as this may also highlight expected signs associated with muscle fiber dysfunction. Last, chemical changes in the cell may be important to understanding the relationships between muscle fiber damage and clinically observable signs. This may include the leak of intramuscular proteins (e.g., creatine kinase enzymes) into the plasma, the loss of intracellular Ca2+ (excessive intracellular Ca2+ and leakage into the plasma), indicators of inflammation such as mast cell granules, and an increase in detectability of CGRP (109, 121, 122). Discussed below, the chemical changes associated with myalgia and trigger points are very similar to those found after eccentric exercise. In brief, eccentric exercise results in muscle fiber damage and observable signs similar to those noted in association with trigger points, and may aid in creating a general model of muscle fiber dysfunction and symptom development. 

NADH stain of "moth-eaten" muscle fibers.

NADH stain of "moth-eaten" muscle fibers.

Myalgia, Metabolic Crisis and Muscle Fiber Changes

  • Reduction in blood flow/Hypoxia
    • Signs of metabolic/energy crisis
    • Moth-eaten fibers and degeneration
  • Muscle fiber type proportion change
    • Taut bands and palpable nodules
    • Type I fiber hypertrophy
    • Increase in Type IIA fibers
    • Increase in transitional fibers
    • Preferential loss of Type I and/or Type II motor units
    • Infiltration of adipose and/or connective tissue

The relationship between repetitive stress, muscle contraction, a reduction in local blood flow, hypoxia and myalgia has been well established (52 - 56, 124, 125, 150). It is likely that hypoxia results in metabolic crisis, as evidenced by correlations between myalgia and the presence of cytochrome c oxidase deficiency (127, 128), excessive ACh at motor endplates (190), and deleterious changes to the mitochondrial and sarcotubular system (126 - 129). Further, metabolic crisis may also explains the appearance of ragged red fibers and moth-eaten fibers which are indications of structural damage to the cell membrane and mitochondria (109, 129, 136). Metabolic crisis may result in necrosis, which could explain the atrophy associated with chronic injury (125 - 127). Further, studies have noted that fatigue and muscle fiber degeneration are higher from constant low-load activities than intermittent activities (even after 30 minutes of rest) (57, 145, 146), which would be better explained by metabolic crisis than the simple depletion of metabolic substrates.

When these events are chronic they lead to further adaptation that may exacerbate blood flow restriction. Cellular changes associated with muscle fiber dysfunction have been correlated with narrowed space between fibers, taut bands and localized abnormal contraction sites that are hypothesized to cause the palpable nodules associated with trigger points (196 - 203). This narrowed space between bands and local over-activity may further increase energy demand and further restrict blood flow. Perhaps in the bodies attempt to adapt, myalgia is associated with type I fiber hypertrophy; however, hypertrophy is paired with a reduction in capillary to fiber cross-sectional area ratio (125 - 127), which in-turn contributes to further hypoxia.

Metabolic issues may also result in fiber type proportion changes. An increase in type IIA fibers has been associated with myalgia (128). Research has also demonstrated that hybrid fibers are more common in muscles undergoing significant adaptation to training or injury, which may explain some of the type IIA fiber increase (130 - 136). Studies also show that low-back pain and cervical pain lead to a preferential reduction in type I fibers in some paraspinal muscles (137 - 139), while the multifidus or upper trapezius exhibit a preferential loss of type II fibers (127, 140 - 143). The potentially opposing findings may represent the attempt of muscle fiber to increase endurance (transition from type IIB/X to IIA) while maintaining strength (transition from type I to type IIA), despite an over-all loss of motor units. Or, it may suggest that different muscles adapt differently to dysfunction, for example a difference may be noted between commonly over-active and under-active muscles. Another interesting maladaptation is some muscles maintain cross sectional area despite the loss of muscle fibers, implying hypertrophy of the remaining fibers, and/or adipose/connective tissue infiltration (137, 143). Despite significant cellular changes and altered fiber type percentages, cross-sectional areas appear to return to near normal values with longer-term/rehabilitation programs (3 weeks-3 years) (147 - 149). Further study is needed to determine whether early intervention may reduce atrophy, and whether intervention may aid in returning normal fiber type proportions.

Chemical Changes involved in Trigger Points

Chemical Changes:

  • Markers of inflammation and pain
  • Acidity (pH)
  • Excessive Ca2+
  • Excessive acetylcholine (ACh)

Significant chemical changes may contribute to the structural changes noted above, and these chemical changes have been correlated with both excessive stress and observable phenomena. These chemical changes can be broken down into three broad categories for the purposes of explanation; however, the human movement professional should be aware that these processes are happening concurrently and influence one another. An increase in pain and inflammatory markers, including acidity, has been correlated with sensitization or stimulation of nociceptors (140 - 164) and may play a special role in explaining myalgia. The cascade resulting from excessive Ca2+ may explain atrophy (124 - 152), moth-eaten fibers, and a decrease in the number of motor units associated with chronic muscle fiber dysfunction. Last, an increase in acetylcholine (ACh), ACh pooling, and or inhibition of acetylcholinesterase (AChE) (153 - 158) may explain taut bands, palpable nodules and some of the change in electric activity discussed in the next section. The following paragraphs will discuss these changes in more detail.

Markers of Inflammation and Pain

Increase in the presence of chemicals, proteins and neurotransmitters related to inflammation, pain and sensitization have been associated with exercise induced cell damage, myalgia and trigger points (109, 122, 168 - 189). This includes calcitonin gene-related peptide (CGRP), bradykinin, substance P, nerve growth factor (NGF), tumor necrosis factor-α (TNF-a), interleukin-1β, interleukin - 6 (IL-6), Interleukin 8 (IL-8), prostaglandin E2 (PGE2), serotonin (including muscle 5 - HT), glutamate, norepinephrine (NE), N-Acylethanolamines (NAEs) and increased macrophage and phagocyte activity (109, 122, 168 - 188). Many of the newer discoveries have been made possible thanks to the development of a "microdialysis" technique, allowing for the sampling of the chemical environment of muscle cells in real time (122, 169, 170,  173, 174, 179 - 189). One such study by Olausson et al. identified 48 proteins with at least two-fold concentrations in those with trapezius myalgia (187), alluding to the immense potential of this technique to add to our understanding. Although a thorough review of the inflammatory cascade resulting from tissue injury and its role in myalgia is beyond the scope of this article, the review by Shah et al. is recommended (179). Some key points deserve mention here. The pro-inflammatory chemical mentioned above, such as tumor necrosis factor alpha (TNF-a), Interleukin 1-beta (IL-1β), Interleukin 6 (IL-6), and Interleukin 8 (IL-8) have been shown to induce hypernociception (175). This may explain the increased sensitivity to pressure and pain associated with active trigger points. The study by Shah et al (169) used microdialysis to demonstrate that many of the chemicals listed above are present at active trigger points sites, but are not present at latent trigger points sites - demonstrating differentiation (170, 171). A study by Hayashi et al. correlated the up-regulation of NGF receptors with chronically painful taut bands (172), aiding in understanding the development of this palpable phenomenon. Studies by Roatta et al. and Shwarz et al. demonstrated that NE affects muscle spindle activity (102, 178), which may have implications regarding the maladaptive length changes noted, relative trigger points and postural dysfunction. Last, a study by Hsieh et al. demonstrated that dry needling positively affected the chemical environment of an identified trigger point in an animal study (188), and Moraska et al. demonstrated positive changes in the chemical environment post ischemic compression (189). As these studies demonstrate, the ability to investigate chemical changes in the environment of the muscle cell aids in associating the pathobiological processes with observable phenomenon, and hopefully will aid in optimizing intervention selection in the future.

Acidity (pH)

Several studies have noted that an increase in tissue acidity can result in pain, specifically within muscle fibers (205 - 209). The microdialysis study by Shah et al., as well as an older study (1957) on "fibrositic muscles" by Brendstrup et al. have demonstrated that the chemical environment of dysfunctional muscle fibers is acidic (lower pH) (170, 210). Studies have specifically demonstrated that creating an acidic environment may stimulate receptors that result in the perception of pain (205 - 206). Although the perception of pain via an increase in acidity is likely the result of stimulating vallinoid receptors, others have modeled more complex links between acidity and local myalgia (207 - 209).

Excessive Calcium Ions (Ca2+)

One of the earliest found and most consistent findings in research investigating muscle fiber dysfunction is an increase in the release of Ca2+ into the muscle cell (109, 151 - 167). Ca2+ is a second messenger for a range of processes in all muscle, and overload may lead to a cascade of events best summarized by Gissel (152): "If the permeability of the sarcolemma for Ca2+ is increased, the muscle cell may suffer Ca2+overload, defined as an inability to control [Ca2+]c. This could lead to the activation of calpains, resulting in proteolysis of cellular constituents, activation of phospholipase A2(PLA2), affecting membrane integrity, an increased production of reactive oxygen species (ROS), causing lipid peroxidation, and possibly mitochondrial Ca2+ overload, all of which may further worsen the damage in a self‐reinforcing process." Evidence of CA2+ overload and the resulting cascade are well supported, and CA2+ overload has been correlated with a range of events including acute trauma, myalgia, low-load continuous activity, and eccentric contractions (excessive exercise) (151 - 161). As this process may result insignificant damage, rupture of the cell membrane, and even necrosis, this process may be a primary contributor to the atrophy, moth-eaten fibers, and decreased number of motor units associated with muscle fiber dysfunction.

Excessive Acetylcholine (ACh)

Evidence of excessive ACh at motor endplates has been correlated with hypoxia (190). Further, CGRP seems to affect both the production of ACh and potentially inhibit the release of Acetylcholinesterase (AChE) resulting in excessive pooling at the motor endplate (192, 193). Note, an increase in CGRP has been associated with myalgia and triggerpoints as mentioned above (170, 175, 176). Several studies have noted the ability of ACh to stimulate nociceptors and pain via purigenic receptors, especially when ACh is leaked from damaged muscle cells (194, 195). Of particular interest, a study by Mense et al., demonstrates an increase in regional ACh results in localized abnormal contraction sites, which are thought to be essential to the formation of the palpable nodule of myofascial trigger points (198). See the images below of electron microscopy of localized abnormal contraction sites hypothesized to contribute to the palpable nodule associated with trigger points. This study adds to our current understanding regarding palpable phenomenon which includes studies that have correlated muscle fiber dysfunction with narrowed space between fibers, local fiber hypertrophy, and palpable taut bands (198 - 203). Understanding the role excessive ACh plays in muscle fiber dysfunction aids in understanding myalgic phenomenon, palpable phenomenon, and electromyographic change discussed below.

Electron microscopy image of local contractile disks in sacromere of several adjacent muscle fibers.

Mense, S., Simons, D. G., Hoheisel, U., & Quenzer, B. (2003). Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation. Journal of applied physiology, 94(6), 2494-2501.

Characteristic Electric Activity of Trigger Points

The characteristic electric activity of trigger points is not easily differentiated from "normal endplate noise", but research does indicate tendencies toward higher amplitude spikes and higher mean activity (210). The difficulty in differentiating the endplate noise associated with trigger points and asymptomatic muscle fibers may be the reason why some studies have failed to note a difference (211). It is likely that the false assumptions that endplate noise and spontaneous activity were normal, not considering the prevalence of muscle fiber dysfunction and trigger/tender points, resulting in a lack of comparison studies until the mid-1990's (212, 213). Hubbard et al. (1993), first demonstrated spontaneous discharges in the order of 10-50 μV and intermittent high-amplitude discharges (up to 500 μV) in painful trigger points that were absent in non-trigger points (214). Since that study, several studies comparing trigger points and normal muscle fibers have demonstrated trigger points exhibit more high amplitude discharges, more instances of spontaneous electric activity, more instances of twitch response and significantly higher root mean square activity (214 - 221). The activity and ensuing muscle fiber action may be similar to "cramping contractions or cramp potentials", sometimes noted by experienced electromyographers (222 - 225).

The number of studies correlating endplate dysfunction with trigger points, and the number of studies either purposefully or coincidentally locating trigger points at the motor endplate, implies that trigger points may be symptoms arising at dysfunctional motor endplates (234). Comparing motor point maps to trigger point maps provides a great visual representation of this trend (232 - 234).

  • 232. Botter, A., Oprandi, G., Lanfranco, F., Allasia, S., Maffiuletti, N. A., & Minetto, M. A. (2011). Atlas of the muscle motor points for the lower limb: implications for electrical stimulation procedures and electrode positioning. European journal of applied physiology111(10), 2461.
  • 233. Behringer, M., Franz, A., McCourt, M., & Mester, J. (2014). Motor point map of upper body muscles. European journal of applied physiology114(8), 1605-1617.

Although some of this activity can be attributed to chemical changes (excessive ACh), Hong et. al noted that trigger points are likely the result of an integrated response that includes the spinal cord responding to sensitized nerve fibers associated with abnormal endplates (226). Kuan et al. published an eloquent example of this relationship, demonstrating the amount of endplate noise at a trigger point was highly correlated with the level of pain pressure threshold (218). Two studies demonstrate that injection of glutamate (neurotransmitter associated with pain receptors) induced higher peak pain intensity and increased EMG activity when injected into trigger points, but did not when saline solution was used, or when glutamate was injected into latent trigger points or asymptomatic fibers (227, 228). Two studies by Fricton et al. and Wang et al. demonstrate higher electric activity associated with taut bands and the twitch response associated with trigger points, both being neuromuscular phenomenon (219, 226). Another study by Ge et al., demonstrated that trigger points exhibit higher H-reflex amplitude and lower H-reflex threshold (electrically induced stretch reflex), than non-MTrPs respectively, suggesting that muscle spindle afferents may be involved in their pathophysiology (230). These studies demonstrate that changes in EMG are likely influenced by changes at the motor endplate, as well as by adaptation from the nervous system.

An interesting study relative to practice: A study by Haung et al., used a trigger point inducing protocol on rats (contusion followed by 8 weeks of eccentric exercise), and demonstrated that the EMG activity associated with trigger points did not resolve in the 12 week follow up (231). This may imply that trigger points are unlikely to resolve without intervention.

Diagram of Spinal Cord Cross Section

Note: Dorsal Horn and Posterior Horn are synonyms.

Muscle Fiber Dysfunction, Pain and the Nervous System

The paragraphs on "Markers of Inflammation and Pain" and "Characteristic Electric Activity and Trigger Points" alluded to the integrated relationship between the muscle fiber, the motor endplate and the nervous system. Additional research demonstrates a relationship between muscle fiber dysfunction and neuromuscular reflex at the level of the spinal cord, how the CNS may adapt to myalgia, and how the autonomic nervous system effects activity and sensitivity of trigger points (latent or active).

Spinal Cord:

The connection between trigger points and the spinal cord has been demonstrated in several studies. A series of animal studies by Hong et al. used a combination of transection and lidocaine blocks to demonstrate that spontaneous electric activity may be produced by the motor endplate alone; however, the twitch response relies on a connection between the muscle fiber and the spinal cord via a motor nerve (235 - 238). Hong et al. also demonstrated that transection of the spinal cord above the level of the tested nerve did not abolish the twitch response, implying this response is reflex mediated by the spinal cord, and higher CNS function is not necessary (236). Perhaps the connection these studies imply also aids in explaining why botulinum toxin A reduces electric activity and the increased number of nerve sprouts at the motor endplate, but is not effective for reducing pain at trigger points (239 - 241). For example, it may be hypothesized that botulinum toxin A addresses the local contributors to endplate potentials, but has little or no effect on the nervous system mediated contributors to myalgia. Additional studies add details to the relationship between the the spinal cord and trigger points. Fernandez-Carnero et al. demonstrated glutamate induced pain of a distal latent trigger point increased electric activity of latent trigger points in a proximal muscle at the same segmental level of the spine (teres major and extensor carpi radialis) (229). Further, Audette et al. demonstrated that needle stimulation of a unilateral upper trapezius active trigger point resulted in bilateral (mirror-image) electromyographic activity (242). Srbely et al. demonstrated the administration of a topical cream at the infraspinatus dermatome increased pain pressure threshold (decreased sensitivity) of infraspinatus trigger points, but had no affect on glute trigger points (243). In an additional study, Srbely et al. demonstrated that dry needling had an anti-nociceptive effect on trigger points related to the same segmental level of the spine (244). These studies may indicate reflexive changes to dorsal horn neurons resulting in increased/decreased thresholds, or reorganization including unmasking of receptive neurons. All of these studies indicate that stimulating a twitch response and/or pain at a trigger point must involve the muscle fiber, peripheral nerves and the spinal cord.

Evidence of Centralization (CNS Adaptation):

There is a significant amount of evidence to suggest trigger points result in centralization. In addition to the pain experience requiring higher CNS functions for perception, studies have demonstrated that affecting one trigger point changes the sensitivity and activity of other distal trigger points. This includes the studies mentioned above by Fernandez-Carnero et al., Audete et al. and Srbely et al (229, 242 - 244) that may or may not require higher CNS functions, and a study by Hsieh et al. in which dry needling of forearm muscles not only decreased trapezius trigger point sensitivity, a significant increase in cervical range of motion was also noted (245). Note, the forearm muscles, trapezius and many of the cervical muscles are not innervated by the same segment. Further, a study by Chou et al. demonstrated that acupuncture to remote sites was capable of reducing endplate noise and pain pressure sensitivity of distal trigger points (254).

Referral pain patterns also allude to involvement of the CNS in muscle fiber dysfunction. A study by Wang et al. demonstrated that injecting glutamate into a trigger point increased the area of pressure induced pain (246). The increase in area must be the result of nervous system adaptations increasing sensitivity of additional afferents. Studies by Hoheisel et al. and Niddam et al. suggest that the nervous system accomplishes this adaptation by reorganizing dorsal horn neurons (including unmasking of receptive neurons), and suppressing activity of the hippocampus (247 - 249). Graven-Nielsen et al. demonstrated that experimental muscle pain is influenced by temporal and spatial summation, and Hoheisel et al. and Meng et al. demonstrated dorsal horn reorganization (within a few hours) (110, 247, 248, 249). Additionally, Gibson et al. demonstrated that sensitivity and the area of pressure induced pain, increased more when trigger points were injected after a delayed onset muscle soreness (DOMS) inducing protocol (252). These studies may have important implications for long-duration, low-load excessive stressors, in which a painful stimulus is repeated often, for long duration, and may continue to increase after the initial onset of pain. In a study with significant practical implications, Rubin et al. demonstrated that continued stimulation of a myalgic point resulted in continued propagation of the referral pain pattern, but that anesthetizing the original site of pain reduced both trigger point pain and referral pain in parallel (in most cases) (253).  These studies suggest that a painful stimulus (trigger point), especially when initiated in addition to other painful experiences and/or initiated often, may results in brain and spinal cord adaptations that increase the painful area and sensitivity.

Autonomic Nervous System and Trigger Points

The effect of breathing, emotional stress, mental stress, and other phenomenon suggest the autonomic system may influence, and be influenced by, trigger points and myalgia. Ge et al. demonstrated that pain pressure threshold was higher at active trigger points when patients were asked to take and hold a deep breath when compared to normal respiration (83). Studies by Lewis et al. and McNulty et al. demonstrated that EMG activity of trigger points increased with emotional and mental stress (255, 256), and Banks et al. demonstrated that relaxation training reduced sensitivity of active trigger points (257). Zhang et al. and Abbaszadeh-Amirdehi et al. demonstrated attenuated skin blood flow response after painful stimulation of latent trigger points when compared to non trigger points, suggesting an increase in sympathetic vasoconstriction (258, 259). Further, phentolamine injection, an epinephrine and norepinephrine antagonist, reduced spontaneous electric activity from trigger points (260). The body of research investigating spinal cord reflex, CNS adaptation and autonomic nervous system involvement demonstrate the integration between muscle fiber dysfunction and the nervous system, and furthers the holistic nature of the human movement system.

The 18 points associated with Fibromyalgia Syndrome Diagnosis - By Sav vas, Jmarchn - Own work, based on: https://commons.wikimedia.org/wiki/File:Tender_points_fibromyalgia.gif, CC0, https://commons.wikimedia.org/w/index.php?curid=21328615

The 18 points associated with Fibromyalgia Syndrome Diagnosis - By Sav vas, Jmarchn - Own work, based on: https://commons.wikimedia.org/wiki/File:Tender_points_fibromyalgia.gif, CC0, https://commons.wikimedia.org/w/index.php?curid=21328615

Fibromyalgia and Whiplash Syndrome

Fibromyalgia syndrome (FS) and whiplash syndrome (WS) deserve their own courses and individual literature reviews; however, a brief summary of their relationship to myalgia and trigger points is given here. Although FS is a chronic condition of insidious onset, and WS syndrome is a chronic condition of traumatic onset, the perpetuating chronic pain that is common to both conditions may be related to centralization of trigger point pain and reinforcement from active trigger points.

Bennet et al. notes, "Central sensitization has to have an initial genesis, and nociceptive stimuli from painful foci in muscle are increasingly recognized as being relevant to the development of fibromyalgia" (261). Based on relevant research, it seems likely that the "painful foci" are active trigger points. Ge et al. demonstrated that FS patients exhibited increased sensitivity, more bilateral trigger points, and more trigger points overall when compared to healthy controls (264). Further, Alonso-Blonco et al. and Ge et al. demonstrated that the widespread spontaneous pain pattern in FS may be reproduced by the stimulation of active trigger points and summation of their painful regions (262, 263). Widespread pain and testing positive for 11 of 18 common active trigger points has a sensitivity of 88.4% and a specificity of 81.1% for the diagnosis of FS (266). All of these studies allude to the strong correlation between trigger points and FS development.

The inclusion of both trigger points and widespread pain in the diagnosis of FS, alludes to the relevance of trigger points and central sensitization. This does create diagnostic issues, as further testing may be necessary to differentiate FS from myofascial pain syndrome (MPS). These difficulties may be anticipated based on the studies mentioned above that demonstrate painful states and stress (as noted in MPS) which are likely to increase trigger point sensitivity and EMG activity (228, 252, 255, 256, 266, 267). Factors alluding to centralization that may aid in differentiating FS from MPS include the "wind-up sensation" (increase in pain with repeated stimulus) and decreased withdrawal reflex threshold (265, 268). The "wind-up sensation" has been correlated with FS and not MPS (268), and seems to allude to the temporal summation and sensitization discussed above under "Centralization and Trigger Points" (250, 251). Additionally, Banic et al. demonstrated decreased stimulation threshold for the withdrawal reflex in those individuals diagnosed with FS and WS (265). These centralized factors may be an effective method for differentiating FS from MPS. Further research is needed to better understand centralized pain, and create better diagnostic criteria for FS.

The prevalence of myalgia complaints by those diagnosed with whiplash syndrome (WS) is high; roughly 80% according to a study by Schuller et al (272). Further, WS has been correlated with an increase in cervical muscle activity and a loss of range of motion (ROM), and if these changes persist the likelihood of full recovery is reduced (273, 274). These changes are signs of muscle fiber dysfunction, but further research also suggests trigger point involvement (79). Several studies have noted that increased sensitization is a feature of WS, especially in those with moderate to severe symptoms at onset, and is correlated with the persistence of symptoms in those who do not fully recover by 6 months (79, 265, 275). This includes the study by Banic et al. mentioned above, that demonstrated that WS and FS patients exhibited a decreased threshold for the withdrawal reflex (209). Further research is needed to investigate whether the myalgic area described by patients with WS can be mimicked by summating the area of active trigger points and their referral pain patterns, as was noted in FS. A study by Sterling et al. demonstrated the persistence of WS symptoms were correlated with greater psychological distress (276), which may be similar to the effect mental and emotional changes have on trigger point sensitivity (228, 252, 255, 256, 266, 267). Although the onset of WS is different than FS, and the research on each condition has focused on different factors, the similarities are worth investigating in pursuit of optimal treatment options for chronic centralized pain.

The study mentioned above by Rubin et al., demonstrated that treatment of referral pain may not be necessary, as trigger point injection reduced referral pain in parallel (253). Similar findings have been noted relative for fibromyalgia; Staud et al. and Giamberardino et al. demonstrated that trigger point injection was also effective for reducing overall fibromyalgia pain, including secondary heat hyperalgesia (268 - 270). Note, Staud et al. emphasized that focus should be placed on active trigger points and not necessarily tender points (269). Manual treatment of trigger points (in conjunction with cervical manipulation) has also been shown to produce better outcomes than modalities for WS (80, 81). Although centralization alludes to the difficulty in reducing symptoms long-term, these studies may provide some hope that continued treatment of trigger points will reduce the painful stimulus and eventually reverse the adaptations resulting in centralized pain.

These studies provide additional insight into the interaction between the nervous system and muscle fiber dysfunction, but demonstrate that fibromyalgia and WS are strongly correlated with trigger points and an increase in centralized characteristics. These studies also allude to a strong correlation between fibromyalgia and WS, active trigger points, centralization, and the treatment of trigger points as a means of reversing the perpetual cycle of centralizing pain. Further research is needed, but it seems a hypothesis may be generated that suggests the etiology of fibromyalgia and WS is a continuum that results from untreated/un-addressed stressors, resulting in muscle fiber dysfunction, resulting in active trigger points, resulting in centralization, amplified by further physical, emotional or mental stress over time.

Coming Soon:

Trigger Point Assessment, Palpation, Treatment and Muscle Specific Research


  1. David G. Simons, Janet Travell, Lois S. Simons, Travell & Simmons’ Myofascial Pain and Dysfunction, The Trigger Point Manual, Volume 1. Upper Half of Body: Second Edition,© 1999 Williams and Wilkens
  2. Mense, S. (1997). Pathophysiologic basis of muscle pain syndromes: an update. Physical Medicine and Rehabilitation Clinics8(1), 23-53.
  3. Gerwin, R. D., & Duranleau, D. (1997). Ultrasound identification of the myofacial trigger pointMuscle & nerve20(6), 767-768.
  4. Fricton, J. R., Kroening, R., Haley, D., & Siegert, R. (1985). Myofascial pain syndrome of the head and neck: a review of clinical characteristics of 164 patients. Oral surgery, oral medicine, oral pathology60(6), 615-623.
  5. Tough, E. A., White, A. R., Richards, S., & Campbell, J. (2007). Variability of criteria used to diagnose myofascial trigger point pain syndrome—evidence from a review of the literature. The Clinical journal of pain23(3), 278-286.
  6. Borg-Stein, J., & Simons, D. G. (2002). Myofascial pain. Archives of physical medicine and rehabilitation83, S40-S47.
  7. Harden, R. N., Bruehl, S. P., Gass, S., Niemiec, C., & Barbick, B. (2000). Signs and symptoms of the myofascial pain syndrome: a national survey of pain management providers. The clinical journal of pain16(1), 64-72.
  8. Vecchiet, L., Giamberardino, M. A., Dragani, L., De Bigontina, P., & Albe-Fessard, D. (1990). Latent myofascial trigger points: changes in muscular and subcutaneous pain thresholds at trigger point and target level. J Manual Medicine5, 151-154.
  9. Vecchiet, L., Dragani, L., De Bigontina, P., Obletter, G., & Giamberardino, M. A. (1993). Experimental referred pain and hyperalgesia from muscles in humans. Pain research and clinical management7, 239-249.
  10. Vecchiet, L., Giamberardino, M. A., de Bigontina, P., & Dragani, L. (1994). Comparative sensory evaluation of parietal tissues in painful and nonpainful areas in fibromyalgia and myofascial pain syndrome. In Proceedings of the 7th World Congress on Pain (Vol. 2, pp. 177-185). IASP Press, Seattle, WA.
  11. Vecchiet, L., & Giamberardino, M. A. (1997). Referred pain: clinical significance, pathophysiology, and treatment. Physical Medicine and Rehabilitation Clinics8(1), 119-136.
  12. Hong, C. Z., Kuan, T. S., Chen, J. T., & Chen, S. M. (1997). Referred pain elicited by palpation and by needling of myofascial trigger points: a comparison. Archives of physical medicine and rehabilitation78(9), 957-960.
  13. Flax, H. J. (1995). Myofascial pain syndromes--the great mimicker. Boletin de la Asociacion Medica de Puerto Rico87(10-12), 167-170.
  14. Borg-Stein, J., & Wilkins, A. N. (2006). Soft tissue determinants of low back pain. Current pain and headache reports10(5), 339-344.
  15. Simons, D. G., & Travell, J. G. (1983). Myofascial origins of low back pain: 1. Principles of diagnosis and treatment. Postgraduate Medicine73(2), 66-77.
  16. Melzack, R., Stillwell, D. M., & Fox, E. J. (1977). Trigger points and acupuncture points for pain: correlations and implications. Pain3(1), 3-23.
  17. Hong, C. Z. (2000). Myofascial trigger points: pathophysiology and correlation with acupuncture points. Acupuncture in Medicine18(1), 41-47.
    • Prevalence
  18. Chaiamnuay, P., Darmawan, J., Muirden, K. D., & Assawatanabodee, P. (1998). Epidemiology of rheumatic disease in rural Thailand: a WHO-ILAR COPCORD study. Community Oriented Programme for the Control of Rheumatic Disease. The Journal of rheumatology25(7), 1382-1387.
  19. Fleckenstein, J., Zaps, D., Rüger, L. J., Lehmeyer, L., Freiberg, F., Lang, P. M., & Irnich, D. (2010). Discrepancy between prevalence and perceived effectiveness of treatment methods in myofascial pain syndrome: results of a cross-sectional, nationwide survey. BMC musculoskeletal disorders11(1), 32.
  20. Skootsky, S. A., Jaeger, B., & Oye, R. K. (1989). Prevalence of myofascial pain in general internal medicine practice. Western Journal of Medicine151(2), 157.
  21. Marklund, S., & Wänman, A. (2008). Incidence and prevalence of myofascial pain in the jaw–face region. A one-year prospective study on dental students. Acta Odontologica Scandinavica66(2), 113-121.
  22. Schmitter, M., Balke, Z., Hassel, A., Ohlmann, B., & Rammelsberg, P. (2007). The prevalence of myofascial pain and its association with occlusal factors in a threshold country non-patient population. Clinical oral investigations11(3), 277-281.
  23. Han, T. I., Hong, C. Z., Kuo, F. C., Hsieh, Y. L., Chou, L. W., & Kao, M. J. (2012). Mechanical pain sensitivity of deep tissues in children-possible development of myofascial trigger points in children. BMC musculoskeletal disorders13(1), 13.
  24. Andersen, J. H., Kærgaard, A., & Rasmussen, K. (1995). Myofascial pain in different occupational groups with monotonous repetitive work. J Musculoskeletal Pain3(Suppl 1), 57.
  25. Chen, S. M., Chen, J. T., Kuan, T. S., Hong, J., & Hong, C. Z. (2000). Decrease in pressure pain thresholds of latent myofascial trigger points in the middle finger extensors immediately after continuous piano practice. Journal of Musculoskeletal Pain8(3), 83-92.
  26. Treaster, D., Marras, W. S., Burr, D., Sheedy, J. E., & Hart, D. (2006). Myofascial trigger point development from visual and postural stressors during computer work. Journal of electromyography and kinesiology16(2), 115-124.
  27. Yoo, W. G. (2013). Changes in pressure pain threshold of the upper trapezius, levator scapular and rhomboid muscles during continuous computer work. Journal of physical therapy science25(8), 1021-1022.
  28. Bajaj, P., Bajaj, P., Graven-Nielsen, T., & Arendt-Nielsen, L. (2001). Trigger points in patients with lower limb osteoarthritis. Journal of Musculoskeletal Pain9(3), 17-33.
  29. Bron, C., Dommerholt, J., Stegenga, B., Wensing, M., & Oostendorp, R. A. (2011). High prevalence of shoulder girdle muscles with myofascial trigger points in patients with shoulder pain. BMC musculoskeletal disorders12(1), 139
  30. Fernández-Carnero, J., Fernández-de-las-Peñas, C., de la Llave-Rincón, A. I., Ge, H. Y., & Arendt-Nielsen, L. (2008). Bilateral myofascial trigger points in the forearm muscles in patients with chronic unilateral lateral epicondylalgia: a blinded, controlled study. The Clinical journal of pain24(9), 802-807.
  31. Weiner, D. K., Sakamoto, S., Perera, S., & Breuer, P. (2006). Chronic low back pain in older adults: prevalence, reliability, and validity of physical examination findings. Journal of the American Geriatrics Society54(1), 11-20.
  32. Rosomoff, H. L., Fishbain, D., Goldberg, M., & Steele-Rosomoff, R. (1990). Myofascial findings in patients with''chronic intractable benign pain''of the back and neck. Pain Management3(2), 114-118.
  33. Cerezo-Téllez, E., Torres-Lacomba, M., Mayoral-del Moral, O., Sánchez-Sánchez, B., Dommerholt, J., & Gutiérrez-Ortega, C. (2016). Prevalence of myofascial pain syndrome in chronic non-specific neck pain: A population-based cross-sectional descriptive study. Pain Medicine17(12), 2369-2377.
  34. Muñoz-Muñoz, S., Muñoz-García, M. T., Alburquerque-Sendín, F., Arroyo-Morales, M., & Fernández-de-las-Peñas, C. (2012). Myofascial trigger points, pain, disability, and sleep quality in individuals with mechanical neck pain. Journal of manipulative and physiological therapeutics35(8), 608-613.
  35. Sari, H., Akarirmak, U., & Uludag, M. (2012). Active myofascial trigger points might be more frequent in patients with cervical radiculopathy. European journal of physical and rehabilitation medicine48(2), 237-244.
  36. Calandre, E. P., Hidalgo, J., García‐Leiva, J. M., & Rico‐Villademoros, F. (2006). Trigger point evaluation in migraine patients: an indication of peripheral sensitization linked to migraine predisposition?. European journal of neurology13(3), 244-249.
  37. Fernández‐de‐las‐Peñas, C., Alonso‐Blanco, C., Cuadrado, M. L., Gerwin, R. D., & Pareja, J. A. (2006). Myofascial trigger points and their relationship to headache clinical parameters in chronic tension‐type headache. Headache: The Journal of Head and Face Pain46(8), 1264-1272.
  38. Giamberardino, M. A., Tafuri, E., Savini, A., Fabrizio, A., Affaitati, G., Lerza, R., ... & Mezzetti, A. (2007). Contribution of myofascial trigger points to migraine symptoms. The Journal of pain8(11), 869-878.
  39. Ardic, F., Gokharman, D., Atsu, S., Guner, S., Yilmaz, M., & Yorgancioglu, R. (2006). The comprehensive evaluation of temporomandibular disorders seen in rheumatoid arthritis. Australian dental journal51(1), 23-28.
  40. Fernández-de-las-Peñas, C., Galán-del-Río, F., Alonso-Blanco, C., Jiménez-García, R., Arendt-Nielsen, L., & Svensson, P. (2010). Referred pain from muscle trigger points in the masticatory and neck-shoulder musculature in women with temporomandibular disoders. The Journal of Pain11(12), 1295-1304.
  41. Bedaiwy, M. A., Patterson, B., & Mahajan, S. (2013). Prevalence of myofascial chronic pelvic pain and the effectiveness of pelvic floor physical therapy. The Journal of reproductive medicine58(11-12), 504-510.
  42. Kadefors, R. (1999). Recruitment of low threshold motor-units in the trapezius muscle in different static arm positions. Ergonomics42(2), 359-375.
  43. Minerbi, A., & Vulfsons, S. (2018). 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 medical journal9(3).
  44. Hagg, G. (1991). Static work loads and occupational myalgia-a new explanation modelElectromyographical kinesiology, 141-144.
  45. Johansson, H., Windhorst, U., Djupsjöbacka, M., & Passatore, M. (2003). Chronic work-related myalgia: neuromuscular mechanisms behind work-related chronic muscle pain syndromes. Gävle University Press.
  46. Henneman, E., Somjen, G., & Carpenter, D. O. (1965). Excitability and inhibitibility of motoneurons of different sizes. Journal of neurophysiology28(3), 599-620.
  47. De Luca, C. J., & Forrest, W. J. (1973). Some properties of motor unit action potential trains recorded during constant force isometric contractions in man. Kybernetik12(3), 160-168.
  48. De Luca, C. J., LeFever, R. S., McCue, M. P., & Xenakis, A. P. (1982). Behaviour of human motor units in different muscles during linearly varying contractions. The Journal of physiology329(1), 113-128.
  49. Hagg, G. (1991). Static work loads and occupational myalgia-a new explanation modelElectromyographical kinesiology, 141-144.
  50. Flodgren, G. M., Crenshaw, A. G., Alfredson, H., Fahlström, M., Hellström, F. B., Bronemo, L., & Djupsjöbacka, M. (2005). Glutamate and prostaglandin E2 in the trapezius muscle of female subjects with chronic muscle pain and controls determined by microdialysis. European journal of pain9(5), 511-511.
  51. Person, R. S., & Kudina, L. P. (1972). Discharge frequency and discharge pattern of human motor units during voluntary contraction of muscleElectroencephalography and clinical neurophysiology32(5), 471-483.
    • Restricted Blood Flow
  52. Wisnes, A., & Kirkebø, A. (1976). Regional distribution of blood flow in calf muscles of rat during passive stretch and sustained contraction. Acta Physiologica Scandinavica96(2), 256-266.
  53. Degens, H., Salmons, S., & Jarvis, J. C. (1998). Intramuscular pressure, force and blood flow in rabbit tibialis anterior muscles during single and repetitive contractions. European journal of applied physiology and occupational physiology78(1), 13-19.
  54. Byström, S. E. G., & Kilbom, Å. (1990). Physiological response in the forearm during and after isometric intermittent handgrip. European Journal of Applied Physiology and Occupational Physiology60(6), 457-466.
  55. Sjøgaard, G., Savard, G., & Juel, C. (1988). Muscle blood flow during isometric activity and its relation to muscle fatigue. European journal of applied physiology and occupational physiology57(3), 327-335.
  56. Cagnie, B., Dhooge, F., Van Akeleyen, J., Cools, A., Cambier, D., & Danneels, L. (2012). Changes in microcirculation of the trapezius muscle during a prolonged computer task. European journal of applied physiology112(9), 3305-3312.
  57. Lexell, J., Jarvis, J., Downham, D., & Salmons, S. (1993). Stimulation-induced damage in rabbit fast-twitch skeletal muscles: a quantitative morphological study of the influence of pattern and frequency. Cell and tissue research273(2), 357-362.
  58. Forsman, M., Kadefors, R., Zhang, Q., Birch, L., & Palmerud, G. (1999). Motor-unit recruitment in the trapezius muscle during arm movements and in VDU precision work. International Journal of Industrial Ergonomics24(6), 619-630.
  59. Forsman, M., Birch, L., Zhang, Q., & Kadefors, R. (2001). Motor unit recruitment in the trapezius muscle with special reference to coarse arm movements. Journal of Electromyography and Kinesiology11(3), 207-216.
  60. Forsman, M., Taoda, K., Thorn, S., & Zhang, Q. (2002). Motor-unit recruitment during long-term isometric and wrist motion contractions: a study concerning muscular pain development in computer operators. International journal of industrial ergonomics30(4-5), 237-250.
  61. Zennaro, D., Läubli, T., Krebs, D., Krueger, H., & Klipstein, A. (2004). Trapezius muscle motor unit activity in symptomatic participants during finger tapping using properly and improperly adjusted desks. Human factors46(2), 252-266.
  62. Zennaro, D., Läubli, T., Krebs, D., Klipstein, A., & Krueger, H. (2003). Continuous, intermitted and sporadic motor unit activity in the trapezius muscle during prolonged computer work. Journal of electromyography and kinesiology13(2), 113-124.
  63. Person, R. S., & Kudina, L. P. (1972). Discharge frequency and discharge pattern of human motor units during voluntary contraction of muscleElectroencephalography and clinical neurophysiology32(5), 471-483.
  64. Hoyle, J. A., Marras, W. S., Sheedy, J. E., & Hart, D. E. (2011). Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. Journal of electromyography and kinesiology21(1), 41-48.
  65. Dideriksen, J. L., Farina, D., Baekgaard, M., & Enoka, R. M. (2010). An integrative model of motor unit activity during sustained submaximal contractions. Journal of Applied Physiology108(6), 1550-1562.
  66. Westgaard, R. H., & De Luca, C. J. (1999). Motor unit substitution in long-duration contractions of the human trapezius muscleJournal of neurophysiology82(1), 501-504.
  67. SØGaard, K. (1995). Motor unit recruitment pattern during low‐level static and dynamic contractions. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine18(3), 292-300.
  68. Søgaard, K., Christensen, H., Jensen, B. R., Finsen, L., & Sjøgaard, G. (1996). Motor control and kinetics during low level concentric and eccentric contractions in man. Electroencephalography and Clinical Neurophysiology/Electromyography and Motor Control101(5), 453-460.
    • Contributing Factors to Continuously Active Motor Units
  69. Westgaard, R. H., & De Luca, C. J. (2001). Motor control of low-threshold motor units in the human trapezius muscle. Journal of neurophysiology, 85(4), 1777-1781.
  70. Proske, U., & Morgan, D. L. (1984). Stiffness of cat soleus muscle and tendon during activation of part of muscleJournal of Neurophysiology52(3), 459-468.
  71. Ounjian, M., Roy, R. R., Eldred, E., Garfinkel, A., Payne, J. R., Armstrong, A., ... & Edgerton, V. R. (1991). Physiological and developmental implications of motor unit anatomy. Journal of neurobiology22(5), 547-559.
  72. Monti, R. J., Roy, R. R., Hodgson, J. A., & Edgerton, V. R. (1999). Transmission of forces within mammalian skeletal muscles. Journal of biomechanics32(4), 371-380.
  73. Petit, J., Filippi, G. M., Emonet-Denand, F., Hunt, C. C., & Laporte, Y. (1990). Changes in muscle stiffness produced by motor units of different types in peroneus longus muscle of cat. Journal of Neurophysiology63(1), 190-197.
  74. Petit, J., Filippi, G. M., Gioux, M., Hunt, C. C., & Laporte, Y. (1990). Effects of tetanic contraction of motor units of similar type on the initial stiffness to ramp stretch of the cat peroneus longus muscleJournal of neurophysiology64(6), 1724-1732.
  75. Altringham, J. D., & Bottinelli, R. (1985). The descending limb of the sarcomere length-force relation in single muscle fibres of the frog. Journal of Muscle Research & Cell Motility6(5), 585-600.
  76. Bodine, S., Roy, R. R., Eldred, E. A. R. L., & Edgerton, V. R. (1987). Maximal force as a function of anatomical features of motor units in the cat tibialis anteriorJournal of Neurophysiology57(6), 1730-1745.
  77. Street, S. F. (1983). Lateral transmission of tension in frog myofibers: a myofibrillar network and transverse cytoskeletal connections are possible transmitters. Journal of cellular physiology114(3), 346-364.
  78. Baker, B. A. (1986). The muscle trigger: evidence of overload injury. J Neurol Orthop Med Surg7(5), 35-44.
  79. Gerwin, R. D., & Dommerholt, J. (2000). Myofascial trigger points in chronic cervical whiplash syndrome. Journal of Musculoskeletal Pain6, 28-28.
  80. Sterling, M., Jull, G., Vicenzino, B., & Kenardy, J. (2003). Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Pain104(3), 509-517.
  81. Fernández-de-las-Peñas, C., Fernández-Carnero, J., Del Cerro, L. P., & Miangolarra-Page, J. C. (2004). Manipulative treatment vs. conventional physiotherapy treatment in whiplash injury: A randomized controlled trialJournal of Whiplash & Related Disorders3(2), 73-90.
  82. de las Peñas, C. F., del Cerro, L. P., & Carnero, J. F. (2005). Manual treatment of post-whiplash injury. Journal of Bodywork and Movement Therapies9(2), 109-119.
  83. Ge, H. Y., Fernández-de-las-Peñas, C., & Arendt-Nielsen, L. (2006). Sympathetic facilitation of hyperalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain. Clinical Neurophysiology117(7), 1545-1550.
  84. Falla, D., Jull, G., Hodges, P., & Vicenzino, B. (2006). An endurance-strength training regime is effective in reducing myoelectric manifestations of cervical flexor muscle fatigue in females with chronic neck pain. Clinical Neurophysiology117(4), 828-837.
  85. Jull, G.A., Falla, D., Vicenzino, B., Hodges, P.W. (2009).  The effect of therapeutic exercise on activation of the deep cervical flexor muscles in people with chronic neck pain.  Manual Therapy. 14: 696-701.
  86. Falla, D., Jull, G., Russell, T., Vicenzino, B., & Hodges, P. (2007). Effect of neck exercise on sitting posture in patients with chronic neck pain. Physical therapy87(4), 408-417.
  87. O’Leary, S., Falla, D., Hodges, P. W., Jull, G., & Vicenzino, B. (2007). Specific therapeutic exercise of the neck induces immediate local hypoalgesia. The Journal of Pain8(11), 832-839.
  88. Falla, D., O’Leary, S., Fagan, A., & Jull, G. (2007). Recruitment of the deep cervical flexor muscles during a postural-correction exercise performed in sitting. Manual therapy12(2), 139-143.
  89. Ge, H. Y., Fernández-de-las-Peñas, C., & Arendt-Nielsen, L. (2006). Sympathetic facilitation of hyperalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain. Clinical Neurophysiology117(7), 1545-1550.
  90. Gunn, C. C., & Milbrandt, W. E. (1976). Tenderness at motor points. A diagnostic and prognostic aid for low-back injury. JBJS, 58(6), 815-825.
  91. Hoyle, J. A., Marras, W. S., Sheedy, J. E., & Hart, D. E. (2011). Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. Journal of electromyography and kinesiology21(1), 41-48.
  92. Fernández‐de‐las‐Peñas, C., Alonso‐Blanco, C., Cuadrado, M. L., Gerwin, R. D., & Pareja, J. A. (2006). Trigger points in the suboccipital muscles and forward head posture in tension‐type headache. Headache: The Journal of Head and Face Pain46(3), 454-460.
  93. Maher, R. M., Hayes, D. M., & Shinohara, M. (2013). Quantification of dry needling and posture effects on myofascial trigger points using ultrasound shear-wave elastography. Archives of physical medicine and rehabilitation94(11), 2146-2150.
  94. Lucas, K. (2007). Effects of latent myofascial trigger points on muscle activation patterns during scapular plane elevation.
  95. Lucas, K. R., Rich, P. A., & Polus, B. I. (2010). Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger pointsClinical Biomechanics25(8), 765-770.
  96. Ge, H. Y., Arendt-Nielsen, L., & Madeleine, P. (2012). Accelerated muscle fatigability of latent myofascial trigger points in humans. Pain Medicine13(7), 957-964.
  97. Sjøgaard, G., Lundberg, U., & Kadefors, R. (2000). The role of muscle activity and mental load in the development of pain and degenerative processes at the muscle cell level during computer work.
  98. Chen, B. M., & Grinnell, A. D. (1997). Kinetics, Ca2+ dependence, and biophysical properties of integrin-mediated mechanical modulation of transmitter release from frog motor nerve terminals. Journal of Neuroscience17(3), 904-916.
  99. Grinnell, A. D., Chen, B. M., Kashani, A., Lin, J., Suzuki, K., & Kidokoro, Y. (2003). The role of integrins in the modulation of neurotransmitter release from motor nerve terminals by stretch and hypertonicity. Journal of neurocytology32(5-8), 489-503.
  100. Kashani, A. H., Chen, B. M., & Grinnell, A. D. (2001). Hypertonic enhancement of transmitter release from frog motor nerve terminals: Ca2+ independence and role of integrins. The Journal of Physiology530(2), 243-252.
  101. Mense, S. (2004). Neurobiological basis for the use of botulinum toxin in pain therapy. Journal of neurology251(1), i1-i7.
  102. Schwarz, P. B., Yee, N., Mir, S., & Peever, J. H. (2008). Noradrenaline triggers muscle tone by amplifying glutamate‐driven excitation of somatic motoneurones in anaesthetized rats. The Journal of physiology586(23), 5787-5802.
  103. Vasseljen Jr, O., & Westgaard, R. H. (1997). Arm and trunk posture during work in relation to shoulder and neck pain and trapezius activity. Clinical Biomechanics12(1), 22-31.
  104. Wegner, S., Jull, G., O’Leary, S., & Johnston, V. (2010). The effect of a scapular postural correction strategy on trapezius activity in patients with neck pain. Manual therapy, 15(6), 562-566.
  105. Kwon JW, Son SM, Lee NK. (2015). Changes in upper-extremity muscle activities due to head position in subjects with a forward head posture and rounded shoulders. J Phys Ther Sci. 27: 1739-1742.
  106. Weon, J. H., Oh, J. S., Cynn, H. S., Kim, Y. W., Kwon, O. Y., & Yi, C. H. (2010). Influence of forward head posture on scapular upward rotators during isometric shoulder flexion. Journal of Bodywork and movement therapies14(4), 367-374.
  107. Graven-Nielsen, T., & Arendt-Nielsen, L. (2003). Induction and assessment of muscle pain, referred pain, and muscular hyperalgesia. Current pain and headache reports7(6), 443-451.
  108. Newham, D. J., McPhail, G., Mills, K. R., & Edwards, R. H. T. (1983). Ultrastructural changes after concentric and eccentric contractions of human