What Is Myofascial Pain?

Jul 11, 2018, 12:23 PM by Floria Chae, MD

Guillaume de Baillou, a French clinician and epidemiologist during the 16th century, prepared one of the first manuscripts on arthritis[1] and muscle pain disorders.[2] Kellgren, a British rheumatologist, studied patterns of referred pain in different muscle groups and ligaments of the spine by injecting intramuscular hypertonic saline.[3] Balfour described painful inflamed nodules in 1816. Since then, many terms have been used to describe trigger points (TrPs): fibrosis myofasciitis, muscular rheumatism, rheumatic myositis, myogelosis, myalgia, myofascial pain, and fibromyalgia.[4] Travell and Rinzler published the first summary of specific referral patterns and tenderness from referred trigger points in 1952.[5] Travell and Simons furthered the knowledge regarding myofascial pain in the two-volume work titled Myofascial Pain and Dysfunction, published in 1983. Travell introduced the term myofascial pain syndrome (MPS) to describe pain generated from TrPs in muscles, tendons, skin, fascia, and ligaments.

The term myofascial pain syndrome today indicates a specific condition that is different from other softtissue pain disorders such as fibromyalgia, tendonitis, or bursitis. MPS can be regional or widespread, where pain often crosses multiple dermatomes, and is frequently accompanied by increased tension and decreased flexibility. It can coexist with other pain conditions such as fibromyalgia, radiculopathies, joint dysfunction, migraines, pelvic pain and other urologic syndromes, postherpetic neuralgia, and complex regional pain syndromes.[6]

“It is important to understand the pathophysiology of myofascial pain because it is common and distinct entity from other musculoskeletal disorders.”

MPS affects every age group and is characterized by myofascial TrP (MTrP) and pain. An MTrP is classically defined as “a hyperirritable spot in skeletal muscle that is associated with a hypersensitive palpable nodule in a taut band.”[7] Palpation of MTrP produces local pain as well as referred pain in a known pattern. MTrP can be classified as active or latent: active MTrP causes spontaneous pain and pain on palpation, whereas latent MTrP causes pain only on palpation.[8]

Cinderella Hypothesis

Several hypotheses imply that muscle overload and overuse are required for developing MTrP. The Cinderella hypothesis describes how muscle recruitment patterns during low-level, static exertions may lead to musculoskeletal disorder symptoms. Because smaller, type I muscle fibers are continuously activated and metabolically overloaded, whereas larger motor fibers spend more time inactivated, type I or Cinderella fibers are more susceptible to muscle damage and calcium dysregulation, which are key factors in the formation of TrPs.[9] Research has demonstrated that upper trapezius MTrPs developed after continued typing for as little as 30 minutes, which supports the theory that even low-level static exertions can cause MTrPs.[10]


Electromyographic studies show spontaneous electrical activity (SEA) generated at MTrP loci, which are not seen in surrounding tissue. SEA results from increases in miniature endplate potentials and excessive acetylcholine release.[11] These dysfunctional motor endplates may explain the taut band phenomenon. Others have hypothesized that excessive acetylcholine release sustains a contracture of the muscle fibers and thus increases metabolic demands.[8]

Integrated Trigger Point Hypothesis

Simons introduced the integrated trigger point hypothesis, which ties together several findings to describe a possible sequence of events in the development of MTrPs. An energy crisis perpetuates sustained contracture of the muscle fibers near an abnormal endplate. The excessive acetylcholine release and the sustained sarcomere contracture lead to increased local metabolic demands and compressed capillary circulation. With the decreased blood flow and sources of adenosine triphosphate, muscle fibers remain in a contracted state and are unable to return calcium to the sarcoplasmic reticulum for muscle relaxation.[7] The local hypoxic condition leads to release of ischemic mediators that can sensitize peripheral nociceptors and generate pain.[12]


Muscle nociceptors can comprise up to 50% of muscle nerves. This may explain the severity of pain and tenderness in muscles on palpation. Nociceptors also innervate the connective tissue of muscle fibers. They can be activated by several stimuli, depending on whether they contain chemoreceptors, mechanoreceptors, or thermoreceptors.[13] Active and latent MTrPs have biochemical differences, as well as healthy muscle tissue by microdialysis.

In one study, subjects were classified into active (neck pain with MTrP), latent (no neck pain, MTrP present), and normal (no neck pain, no MTrP) groups. Results showed that active MTrPs had acidic pH levels, elevated catecholamines (norepinephrine and serotonin), elevated neuropeptides (substance P [SP] and calcitonin gene-regulated peptide [CRGP]), and elevated cytokines (TNF-a, IL-6, and IL-8) as compared to the latent MTrP and normal groups. After dry needling in the active group, SP and CGRP concentrations were significantly lower than before dry needling. This may be because of increased local blood flow, leading to a washout of pain and inflammatory mediators.[14] Continuous activation of muscle nociceptors by local release of pain mediators from muscle injury and inflammation can induce neuroplastic changes and central sensitization by causing transcriptional changes on the cellular level, leading to hypersensitivity and hyperexcitability.[15]


It is important to understand the pathophysiology of myofascial pain because it is common and distinct entity from other musculoskeletal disorders and is treated differently than other disorders. Studies have confirmed the presence of elevated levels of inflammatory and pain mediators in MTrPs that are not found in normal muscles, supporting the integrated trigger point hypothesis in which an energy crisis and local hypoxic conditions contribute to release of inflammatory and pain mediators that sensitize peripheral nociceptors, leading to central sensitization and pain.


  1. Guillaume de Baillou (1538–1616) clinician and epidemiologist. JAMA. 1966;195(11):957.
  2. Shah JP, Thaker N, Heimur J, et al. Myofascial trigger points then and now: a historical and scientific perspective. PM R. 2015;7:746–761. doi: 10.1016/j. pmrj. 2015.01.024.
  3. Bubnov, V. Evidence-based pain management: is the concept of integrative medicine applicable? EPMA J. 2012;3(1):13. doi: 10.1186/1878-5085-3-13.
  4. Simons DG. Muscle pain syndromes—part 1. Am J Phys Med. 1975;54:289– 311.
  5. Osterwies M, Kleinman A, Mechanic D, eds. Pain and Disability: Clinical, Behavioral, and Public Policy Perspectives. Washington, DC: The National Academies Press; 1987. Available at: Accessed October 22, 2017.
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  7. Simons DG, Travell JG, Simons L. Myofascial Pain and Dysfunction: The Trigger Point Manual. Philadelphia, PA: Lippincott Williams & Wilkins; 1999.
  8. Mense S, Simons DG. Muscle Pain: Understanding Its Nature, Diagnosis, and Treatment. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.
  9. Hagg G. Ny forklaringsmodell for muskelskador vid statisk belastnin i skuldra och nacke [in Swedish; New explanation for muscle damage as a result of static loads in the neck and shoulder]. Arbete Manniska Miljo. 1988;4: 260–262.
  10. Treaster D, Marras WS, Burr D, Sheedy JE, Hart D. Myofascial trigger point development from visual and postural stressors during computer work. J Electromyogr Kinesiol. 2006;16:115–124. doi: 10.1016/j.jelekin.2005.06.016.
  11. Hubbard DR, Berkoff GM. Myofascial trigger points show spontaneous needle EMG activity. Spine. 1993;18:1803–1807.
  12. Huguenin LK. Myofascial trigger points: the current evidence. Phys Ther Sport. 2004;5:2–12. doi: 10.1016/j.ptsp.2003.11.002.
  13. Willard F. Basic mechanisms of pain. In: Audette JF, Bailey A, eds. Integrative Pain Medicine: The Science and Practice of Complementary and Alternative Medicine in Pain Management. New York, NY: Humana Press; 2008:19–61.
  14. Shah JP, Gilliams, EA. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: an application of muscle pain concepts to myofascial pain syndrome. J Bodyw Mov Ther. 2008;12:371–384. doi: 10.1016/j.jbmt.2008.06.006.
  15. Wall PD, Woolf CJ. Muscle but not cutaneous C-afferent input produces prolonged increases in the excitability of the flexion reflex in the rat. J Physiol. 1984;356:443–458.
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