What is myofascial pain? (Proceedings)

Article

Anyone who has suffered from tension headaches, tennis elbow or recurrent back pain has experienced some form of myofascial pain.

Medical practitioners are adept at recognizing and treating the pain associated with internal organ pathology, osteoarthritis, and musculoskeletal injuries, but are less familiar with the chronic pain and dysfunction that arise from myofascial pain syndromes. Anyone who has suffered from tension headaches, tennis elbow or recurrent back pain has experienced some form of myofascial pain.

Eminent researcher David Simons quotes "Muscle is an orphan organ. No medical specialty claims it. As a consequence, no medical specialty is concerned with promoting funded research into the muscular causes of pain, and medical students and physical therapists rarely receive adequate primary training in how to recognize and treat myofascial trigger points." In spite of volumes of scientific literature, studies have demonstrated that primary care physicians are largely ignorant of the diagnosis and treatment of myofascial pain. Students of anatomy are taught to ignore the tough white connective tissue that interferes with visualization of underlying structures, depriving them of the opportunity to appreciate the complex structure and function of fascial tissues.

The term "myofascial" is derived from the root "myo" meaning muscle, and "fascia" defined as a sheet or band of fibrous connective tissue enveloping, separating or binding together muscle, organs or other structures of the body. Myofascial pain is the conscious perception of the stimulation of pain fibers within muscle or fibrous connective tissue that is provoked by the presence of muscle trigger points, or by fascial restrictions that bind, compress or pull on pain sensitive structures. This presentation will focus on the structural and physiologic characteristics of myofascial tissues and relate them to the patho-physiology of muscle trigger points, fascial restrictions and their treatment.

Connective tissue structure and function

The fascial system is an extensive continuous network that imparts organization and form to the body. All other tissues are supported upon (epithelial), invaginated into (glandular epithelium), or imbedded within (muscles, blood vessels and nerves) connective tissue. Connective tissue is composed of cellular (fibroblasts) and extracellular (fibers and ground substance) elements. The functions of connective tissue include mechanical support, independent movement of skin and muscles, transfer of tensile forces, shock absorption, growth and repair, immunological defense (inflammation), transport of nutrients and metabolites, communication, and control of metabolic processes.

Fibroblasts secrete the extracellular matrix. Their long cytoplasmic processes are interconnected and linked in continuous bodywide network. Because of their interconnectedness, it is hypothesized that fibroblasts contribute to a body-wide signaling network.1 Fibroblasts are responsible for growth and repair by producing collagen and secreting the extracellular matrix. Mechanical stimuli, such as stretch, compression, shear and tensile forces determine the location and rate of production of connective tissue components. Fibroblasts respond to mechanical stimuli via a process called mechano-transduction. Mechano-transduction is the process of converting mechanical deformation of a fibroblast's cytoskeletal structure into chemical or electrical signals. The signals alter molecular structure and function inside the cell, activating signaling pathways and altering genetic expression. Mechanical stimuli profoundly affect cell function and behavior.

Ground substance is a gel-like substance that consists of proteoglycan aggregates capable of binding water and electrolytes. Ground substance exhibits the property of thixotropy; the tendency to become more fluid-like when disturbed. Conversely, when static, ground substance becomes more viscous. Increased viscosity limits the degree to which nutrients, oxygen and metabolites are able to diffuse through ground substance, depriving surrounding cells and tissues of vital substances.

Collagen fibers provide the structural framework of connectives tissue. They provide a balance between resistance to tensile forces and mobility of the tissue. Collagen fibers respond to mechanical stimuli by orienting along the lines of stress. Motion deprivation results in random fiber orientation and increased cross-linking between fibers. Consequently, tissue mobility and extensibility are reduced. Thickened, immobile collagen fibers are more susceptible to injury, are painful when stretched and may compress, bind and restrict muscular, vascular and neural elements within them.

Fascial structures are rich in sensory mechanoreceptors, free nerve endings, autonomic innervation and smooth muscle cells. The exact functions of these elements have not been determined, but are the subject of ongoing research. Free nerve endings have a role in pain perception, thus it is likely that pathologic processes within fascia can and does give rise to pain. Fascial contraction independent of motor fiber influence has been observed and is potentially a function of smooth muscle cells. Fascial contraction may play a role in maintaining proper tension in structures such as the lumbar fascia. Mechanoreceptors have a postulated role in kinesthesia, coordination of motor and local autonomic functions and influence of local fluid dynamics.

Painful fascial restrictions are a response to trauma that may be in the form of an acute injury, repetitive micro-stresses, or habitual postural strain or to prolonged immobilization. The fascia loses its flexibility, ground substance becomes more viscous and collagen cross-links proliferate. Elastic properties of elastin diminish. The loss of resiliency affects the quality and quantity of movement; restricted fascia places tension on adjacent structures. Over time structural alignment, biomechanics and strength are affected. Compensatory movement patterns are established to avoid painful and restricted motions. Function and performance subsequently diminish.

Muscle pain and trigger points

Trigger points are defined as "a hyperirritable spot, usually within a taut band of skeletal muscle or in the muscle's fascia, that is painful on compression and that can give rise to characteristic referred pain, tenderness, motor dysfunction and autonomic phenomena."

Trigger points were described by Janet G. Travell, MD, (1901-1997), an internist who became the White House physician under John F Kennedy. She developed a special interest in the treatment of myofascial pain and dysfunction and published the two-volume text Myofascial Pain and Dysfunction: The Trigger Point Manual. The manuals are a comprehensive review of 150 muscle referred-pain patterns and an extensive review of the scientific basis of myofascial trigger points.

Characteristics of trigger points

  • They are hypersensitive to pressure.

  • They refer pain in a pattern that is characteristic of the affected muscle. The referral pattern may follow dermatomal, myotomal, sclerotomal or peripheral nerve distribution patterns. However, the distribution of referred trigger point pain rarely coincides with the entire distribution of a peripheral or spinal nerve segment.

  • They exhibit other referred phenomena including vascular, secretory, pilomotor and autonomic changes.

  • They are self sustaining over long periods of time and they are self-perpetuating, tending to spread to other muscles sharing common innervations.

  • They are detected as a taut band when palpating perpendicular to fiber direction and as a nodule when palpating parallel to fiber direction.

  • They exhibit a transient contraction known as a "local twitch response" in response to snapping palpation or needle penetration.

Sensory effects of trigger points

  • Local tenderness

  • Referral of pain to a distant site.

  • Peripheral sensitization: a reduction in threshold and an increase in responsiveness of the peripheral ends of nociceptors.

  • Central sensitization: an increase in the excitability of neurons within the central nervous system.

  • Sensitization results in

o Allodynia – pain due to a stimulus that does not normally provoke pain

o Hyperalgesia – an increased response to a stimulus that is normally painful

Autonomic effects of trigger points

  • Vasoconstriction, vasodilation, piloerection or lacrimation

  • These effects would occur within the referral zone of the trigger point.

Effects of trigger points on skeletal muscle function

  • Muscles are painful and tender. Pain may be spontaneous or in response to voluntary movement, stretch or palpation.

  • The individual experiences stiffness of the affected muscles.

  • Affected muscles exhibit loss of flexibility and range of motion.

  • There is weakness of affected muscles and diminished EMG activity in the muscle as a whole.

  • The individual actively avoids painful ranges of motion.

  • Compensatory patterns emerge; unaffected muscles are recruited to support movement patterns.

Theories of the etiology of trigger points

  • Prolonged, repetitive motor tasks. Low-level static muscle contractions have been shown to cause structural damage to muscle cells, energy depletion and myalgia.

  • Intramuscular pressures increase during static low-level muscle contractions leading to excessive capillary pressure, decreased circulation and localized hypoxia and ischemia.

  • Acute muscle overload: whiplash, lifting injuries, sports performance or direct trauma.

  • Muscle overload and damage associated with unaccustomed exercise. Overload results in ultra-structural damage at the cytoskeletal level and capillary constriction, muscle hypoxia and ischemia.

Pathophysiologic and electrophysiologic mechanisms of trigger points

A local or proximal inciting event results in prolonged muscle contraction, hypoperfusion, hypoxemia and ischemia. The resultant release of chemical inflammatory mediators contributes to hyperalgesia and perpetuation of the trigger point. In particular, the release of calcitonin gene-related peptide contributes to dysfunction of the motor endplate characterized by an excessive release of acetylcholine and decreased effectiveness of acetylcholinesterase. Excessive acetylcholine affects voltage-gated sodium channels of the sarcoplasmic reticulum and increases the intracellular calcium levels. This results in abnormally contracted regions and uncontrolled shortening of muscle fibers. Myosin filaments in the damaged regions may actually become "stuck", preventing the sarcomere from restoring its resting length. EMG studies of myofascial trigger points demonstrate increased endplate noise within the trigger point compared to areas within the endplate zone but outside the trigger point. Stimulating a trigger point by snapping palpation or needling results in a rapid increase in EMG activity within the trigger point; called the "local twitch response". This phenomenon is grossly visible and palpable.

Histologic and metabolic characteristics of trigger points

Histologically, trigger points consist of a contraction disk that is characterized by an abrupt bulging of the sarcolemma. Within the enlarged area there is a loss of sarcomeres and of normal muscle architecture. The contraction disk is flanked on either side by contracted, shortened sarcomeres. The overall effect is a shortening of the muscle fiber. In addition, biopsies reveal a decrease in quantity of mitochondria indicating metabolic stress.

The local biochemical milieu of trigger points reflects increased concentrations of protons, bradykinin, calcitonon gene-related peptide, substance P, tumor necrosis factor, interleukin 1-B, serotonin and norepinephrine and a lowered pH. These biochemical alterations contribute to muscle hyperalgesia and nociceptor sensitization. Metabolically the tissue experiences diminished oxygen tension, increased temperature, a decrease in high-energy phosphates and a potential decrease in blood supply in the face of increased metabolic demand. A metabolic crisis ensues, which decreases the tissue's ability to cope with anatomical and biochemical derangements.

Musculoskeletal dysfunction

Excessive firing and endplate dysfunction provokes ongoing muscular contraction and eventually results in "shortened muscle syndrome". Histologically, sarcomeres are shortened. Grossly, muscles are tense, contain "ropy bands" and nodules and exhibit loss of range of motion. A hallmark sign is muscle pain and hypersensitivity.

Proposed detrimental effects on musculoskeletal function include

  • Mechanical stress and increased traction at muscle attachments sites resulting in tendonitis (bicipital tendonitis, lateral epicondylitis)

  • If a sesamoid bone is within a shortened tendon compression against the sesamoid increases, resulting in abrasion and pain

  • Compression across joints which increases pressure on cartilage surfaces and alters alignment resulting in uneven forces across the joint; may result in more rapid degenerative changes

  • Shortening of paraspinal muscles across a disc space compresses the disc and narrows the intervertebral foramen potentially exacerbating nerve root compression and muscle shortening

  • Loss of trophic functions affects quality of replacement collagen; it has fewer cross-links, is weaker and is more susceptible to damage from normal wear and tear

  • Mechanical and chemical abnormalities result in primary muscle pain. Painful muscles exhibit lower force production and are weaker. This weakness occurs in the absence of muscle atrophy.

  • Pain and weakness promote compensatory movement patterns; other muscles are substituted and may be over used and improperly used

  • Myofascial tension and fibrotic changes in the muscle may compress local nerves resulting in neuropathic injury.

In conclusion, myofascial tissues are susceptible to dysfunction syndromes that will cause pain even in the absence of overt injury. Pain and dysfunction of these tissues can have significant deleterious effects on biomechanics of movement and locomotion, athleticism, overall health and quality of life. Clinicians need to be aware of the pathophysiology of these syndromes and be able to diagnose and treat those patients suffering from myofascial pain.

Treatment of myofascial pain syndromes will be presented in the following lectures on "Diagnosing and treating myofascial pain in small animals" and "Diagnosing and treating myofascial pain in equine patients".

References

1. Langevin HM, Cornbrooks CJ, Taatjes DJ. Fibroblasts form a body-wide cellular network Histochem Cell Biol 2004;122:7-15.

2. Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual, Vol I. Baltimore, MD; Williams & Wilkins; 1992.

3. Hong CZ, Simons DG. Patholophysiologic and electrophysiologic mechanisms of myofascial trigger points. Arch Phys Med Rehab 1998;79:863-872.

4. Shah JP, Phillips TM, Danoff JV, Gerber LH. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J App Physiol 2005;99:1977-1984.

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