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Muscle Fiber Dysfunction and Trigger Points Audio

Defining trigger points (knots), fibromyalgia, referred pain, tender points, whiplash, chronic low back pain, and postural dysfunction. Review of trigger point development, the impact of trauma and pain, posture, and eccentric loading, and prevalence. Muscle fiber changes, adaptations, soreness development from repetitive stress, muscular contractions, and myalgia. 

Muscle Fiber Dysfunction and Trigger Points

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Over the last years I've returned time and again to Brookbush Institute for stellar coursework as I've worked toward a Human Movement Specialist certification. (I'm currently ACE CPT, and in training with Anatomy Trains for Structural Integration Manual Therapy.) Every Brookbush Institute module is fantastic and each one includes detailed informational videos, written descriptions of how to-do, and, more importantly, why to-do!

I am a 70 yr old chiropractor and no other healthcare provider was able to come up with an exercise protocol particular to my structural and balances and muscle deficits and keep me in the game. And as for continuing education on human skeletal movement, the website is phenomenal full of great exercises for particular mechanical dysfunction.

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We learn principles in academia, we learn cool new modalities via whatever specialty certification, but BBI really concentrates on the nuances of passive treatment and they do a fantastic job. The format in which BBI instructs soft tissue specialists (DPTs, Chiros, ATs) like myself feels like almost like an apprenticeship. You get a thoroughly detailed explanation of the “why’s”, and a visual comprehension of how to apply. Personally, I believe application is where the good and the great are distinguished.

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Human Movement Specialist

Integrated Manual Therapist

This course discusses myofascial trigger points (muscle trigger points) and their relationship to muscle fiber dysfunction. A comprehensive systematic research review is included in this course discussing the prevalence, etiology, observable phenomenon, and pathobiology associated with trigger point development. This course also intends to clarify topics that have been obscured by myth and misinformation, including the definition of trigger points and referral pain patterns, the relationship between trigger points and continuous low-load stress (including posture), and the observable phenomenon that demonstrate the existence and accessibility of trigger points. Further, this course begins to detail the relationship between trigger points and myofascial pain syndrome, chronic whiplash syndrome, and fibromyalgia.

Movement professionals (personal trainers, fitness instructors, physical therapists, athletic trainers, massage therapists, chiropractors, occupational therapists, etc.) should consider this course as introductory, or foundational material for self-administered and manual release techniques. This course is part of our continued effort to build an evidence-based, integrated, systematic, patient-centered, and outcome-driven approach.

"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 the label "herniated nucleus pulposus (HNP)". The gross majority of opposing views on trigger points are based on this 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.

Observable Phenomena Associated with Muscle Fiber Dysfunction:

Changes in muscle spindle activity (H-reflex)

Based on clinical observations, many of these phenomena 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.

Course Description: Muscle Fiber Dysfunction and Trigger Points

Muscle Fiber Dysfunction and Trigger Points Course Study Guide

Study Guide: Muscle Fiber Dysfunction and Trigger Points

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 additional 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 research. Insufficient technology is especially apparent in facets of sports medicine research that involve cellular or molecular processes in living humans.

Pectoralis major tripper point release 

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 may be 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 may contribute but are distinct from FS.

Diagram of the &#34;Integrated Trigger Point Hypothesis&#34; from Dommerholt, J., Bron, C., &amp; Franssen, J. (2006). Myofascial trigger points: an evidence-informed review. Journal of Manual &amp; 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 how terms are defined, used in practice, and what research implies about them. For example, the term "trigger point" should be categorized in a continuum of the 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 the clinically observable phenomena associated with muscle fiber dysfunction that results 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 the fascia (e.g. fasciitis).

Posterior deltoid, upper trapezius, and levator scapulae trigger points

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

Introduction and Definitions

 A general term used to encompass all commonly noted changes resulting from excessive stress to a muscle fiber, and the clinically observable phenomenon that results from those changes.

 Muscle pain, and/or the sub-category of clinically observable phenomena associated with muscle fiber dysfunction that include pain.

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)."

 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 is rarely completely congruent with the distribution of a peripheral nerve or dermatomal segment.

 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 the range of motion (1).

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".

 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).

 Diagnosed pain syndrome that generally includes (4-7):  

Tenderness at points in firm bands of skeletal muscle

Specific patterns of pain referral associated with each point

Frequent emotional, postural, and behavioral contributing factors

Frequent associated symptoms and concomitant diagnoses

 A loosely defined diagnosis that is associated with widespread pain 

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 patient's 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 phenomena from least to most severe, or perhaps in association with least to most muscle fiber damage/maladaptation:

Pathobiology of Muscle Fiber Dysfunction:

Capillary restriction (especially during isometric contraction)

Insufficient recovery (cycling of motor units is insufficient)

Mitochondrial, sarcotubular system, and cell membrane changes

Preferential loss of Type I and/or Type II motor units

Infiltration of adipose and/or connective tissue

A significant amount of research correlates the pathobiology of muscle fiber dysfunction with clinically observable phenomena. 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.

The FHL and FDL common trigger points

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

Additional Definitions, Observable Phenomenon and Pathobiology

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 a 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 women 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.

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 

 OA, and a combined prevalence of 57% in OA patients (28). Studies by Bron et al. demonstrated that 100% of patients with 

 pain exhibited trigger points, with the prevalence of active and latent trigger points varying between muscles of the 

 (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.

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 

 (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 

 (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 

, 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, 

, and suboccipital muscles (40). These studies suggest that the development of trigger points often accompanies head and neck issues.

A significant amount of additional research investigating the prevalence of trigger points as it relates to individual muscles is covered in the "Static Manual Release" courses. The studies above, and additional research investigating individual muscles, implies 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 - muscle fiber dysfunction and trigger points may be evidence of musculoskeletal maladaptation, and a component of an integrated model of dysfunction and pathology that would also include components such as altered muscle recruitment, arthrokinematic stiffness/laxity, fascial dysfunction, inflammation, and pain.

Cervical dysfunction is a common issue for many people who sit at their desk

Prevalence

Common site of knee pain

Trauma and Pain

Running - an example of a continuous low-load activity

Continuous low-load activity

A common dysfunction of forward head position

Posture

NADH stain of moth-eaten muscle fibers

Eccentric Loading

Mechanisms of Excessive Stress

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, a metabolic crisis may also explain 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. Myalgia is also associated with type I fiber hypertrophy; however, hypertrophy is paired with a reduction in the capillary to fiber cross-sectional area ratio (125 - 127), which in turn contributes to further hypoxia. The combination of these adaptations may aid in explaining the changes that result in chronic pain and dysfunction.

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 

 muscles (137 - 139), while the multifidus or 

 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 overall 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.

Myalgia, Metabolic Crisis and Muscle Fiber Changes

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.

An increase in the presence of chemicals, proteins, and neurotransmitters related to inflammation, pain, and sensitization has 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),

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 present in those with 

 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 in muscles exhibiting signs of trigger point development 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 phenomena and hopefully will aid in optimizing intervention selection in the future.

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).

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 muscles, 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 in significant 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.

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 trigger points 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.

Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation

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.

Chemical Changes Correlated with 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 and not considering the prevalence of muscle fiber dysfunction and trigger/tender points, resulted in a lack of comparison studies until the mid-1990s (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).

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 study of this relationship, demonstrating that the amount of endplate noise at a trigger point was highly correlated with the pain pressure threshold (218). Two studies have demonstrated that injection of glutamate (a 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 phenomena (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.

An image of the dorsal horn, anterior horn, and gray commisure

Note: Dorsal Horn and Posterior Horn are synonyms.

Characteristic Electric Activity of Trigger Points

Increase in sensitivity and activity of trigger points at the same segment

Re-organization of dorsal horn neurons and suppression of hippocampus

Decrease/increase in sensitivity and activity when trigger points from a different segment are addressed.

Mental and emotional stress, and relaxation effect trigger point activity and sensitivity

Painful stimulation of latent trigger points results in sympathetic vasoconstriction

Phentolamine (epinephrine and norepinephrine antagonist) decreases trigger point activity

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 affects activity and sensitivity of trigger points (latent or active).

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 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 (

 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 the pain pressure threshold (decreased sensitivity) of 

 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 

 trigger point sensitivity, a significant increase in cervical range of motion was also noted (245). Note, the forearm muscles, 

 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 the 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 the area must be the result of nervous system adaptations increasing the 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 the 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 result 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 phenomena, suggest the autonomic system may influence, and be influenced by, trigger points and myalgia. Ge et al. demonstrated that the 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 

 (258, 259). Further, phentolamine injection, 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.

Common trigger points for individuals with fibromyalgia syndrome

Fibromyalgia and Whiplash Syndrome

Nervous System Adaptations

Static Manual Release: Cervical Muscles Part 1

Static Manual Release: Cervical Muscles Part 2

Static Manual Release: Hip External Rotators

Static Manual Release: Hip Internal Rotators

Static Manual Release: Tibia External Rotators

Additional Courses related to Trigger Points

Mense, S. (1997). Pathophysiologic basis of muscle pain syndromes: an update.

 Physical Medicine and Rehabilitation Clinics 

Gerwin, R. D., & Duranleau, D. (1997). Ultrasound identification of the myofacial trigger point.

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 pathology 

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.

Borg-Stein, J., & Simons, D. G. (2002). Myofascial pain.

 Archives of physical medicine and rehabilitation 

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.

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.

Vecchiet, L., Dragani, L., De Bigontina, P., Obletter, G., & Giamberardino, M. A. (1993). Experimental referred pain and hyperalgesia from muscles in humans.

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.

Vecchiet, L., & Giamberardino, M. A. (1997). Referred pain: clinical significance, pathophysiology, and treatment.

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.

Flax, H. J. (1995). Myofascial pain syndromes--the great mimicker.

 Boletin de la Asociacion Medica de Puerto Rico 

Borg-Stein, J., & Wilkins, A. N. (2006). Soft tissue determinants of low back pain.

Simons, D. G., & Travell, J. G. (1983). Myofascial origins of low back pain: 1. Principles of diagnosis and treatment.

Melzack, R., Stillwell, D. M., & Fox, E. J. (1977). Trigger points and acupuncture points for pain: correlations and implications.

Hong, C. Z. (2000). Myofascial trigger points: pathophysiology and correlation with acupuncture points.

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.

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.

Skootsky, S. A., Jaeger, B., & Oye, R. K. (1989). Prevalence of myofascial pain in general internal medicine practice.

Muscle Fiber Dysfunction and Trigger Points

Related Courses:

Course Description: Muscle Fiber Dysfunction and Trigger Points

Study Guide: Muscle Fiber Dysfunction and Trigger Points

Introduction and Definitions

Additional Definitions, Observable Phenomenon and Pathobiology

Prevalence

Mechanisms of Excessive Stress
4 Sub Sections

Myalgia, Metabolic Crisis and Muscle Fiber Changes

Chemical Changes Correlated with Trigger Points

Characteristic Electric Activity of Trigger Points

Nervous System Adaptations
1 Sub Section

Additional Courses related to Trigger Points

Bibliography

Related Courses:

Comments

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Muscle Fiber Dysfunction and Trigger Points

Related Courses:

Course Description: Muscle Fiber Dysfunction and Trigger Points

Study Guide: Muscle Fiber Dysfunction and Trigger Points

Introduction and Definitions

Additional Definitions, Observable Phenomenon and Pathobiology

Prevalence

Mechanisms of Excessive Stress4 Sub Sections

Myalgia, Metabolic Crisis and Muscle Fiber Changes

Chemical Changes Correlated with Trigger Points

Characteristic Electric Activity of Trigger Points

Nervous System Adaptations1 Sub Section

Additional Courses related to Trigger Points

Bibliography

Related Courses:

Comments

Guest

Mechanisms of Excessive Stress
4 Sub Sections

Nervous System Adaptations
1 Sub Section