Trigger point: Wikis


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Trigger points or trigger sites are described as hyperirritable spots in skeletal muscle that are associated with palpable nodules in taut bands of muscle fibers. [1] Trigger point researchers believe that palpable nodules are small contraction knots and a common cause of pain. Compression of a trigger point may elicit local tenderness, referred pain, or local twitch response. The local twitch response is not the same as a muscle spasm. This is because a muscle spasm refers to the entire muscle entirely contracting whereas the local twitch response also refers to the entire muscle but only involves a small twitch, no contraction.

The trigger point model states that unexplained pain frequently radiates from these points of local tenderness to broader areas, sometimes distant from the trigger point itself. Practitioners claim to have identified reliable referred pain patterns, allowing practitioners to associate pain in one location with trigger points elsewhere. Many chiropractors and massage therapists find the model useful in practice, but the medical community at large has not embraced trigger point therapy. Although trigger points do appear to be an observable phenomenon with defined properties, there is a lack of a consistent methodology for diagnosing trigger points and a dearth of theory explaining how trigger points arise and why they produce specific referred pain patterns.[2]



The term "trigger point" was coined in 1942 by Dr. Janet Travell to describe a clinical finding with the following characteristics:

  • Pain related to a discrete, irritable point in skeletal muscle or fascia, not caused by acute local trauma, inflammation, degeneration, neoplasm or infection.
  • The painful point can be felt as a tumor or band in the muscle, and a twitch response can be elicited on stimulation of the trigger point.
  • Palpation of the trigger point reproduces the patient's complaint of pain, and the pain radiates in a distribution typical of the specific muscle harboring the trigger point.
  • The pain cannot be explained by findings on neurological examination.

One criticism of the trigger point concept is that practitioners do not necessarily agree on what constitutes a trigger point.

A study by Gerwin et al. found that independent examiners were generally able to identify myofascial trigger points (MTrP), but only with sufficient training and agreement on the definition and features of MTrP's. They said:

Three previous studies (Nice et al., 1992; Wolfe et al., 1992; Njoo and Van der Does, 1994) have examined this problem, and none of them could establish the reliability of MTrP examination in all of its major manifestations. ... The present study shows that four examiners can achieve statistically significant agreement, at times almost perfect agreement, about the presence or absence of five major features of the MTrP and on the presence or absence of the TrP, whether it be latent or active. This establishes the MTrP as a reliable clinical sign. The present study also shows that these features are identified with greater or lesser reliability depending on the specific feature and the specific muscle being examined. ... A training period was found to be essential in order to achieve these results.[3]

A 2007 review of diagnostic criteria used in studies of trigger points concluded that

there is as yet limited consensus on case definition in respect of MTrP pain syndrome. Further research is needed to test the reliability and validity of diagnostic criteria. Until reliable diagnostic criteria have been established, there is a need for greater transparency in research papers on how a case of MTrP pain syndrome is defined, and claims for effective interventions in treating the condition should be viewed with caution.[2]

Myofascial pain syndrome

The main innovation of Travell's work was the introduction of the myofascial pain syndrome concept (myofascial referring to the combination of muscle and fascia). This is described as a focal hyperirritability in muscle that can strongly modulate central nervous system functions. Travell and followers distinguish this from fibromyalgia, which is characterized by widespread pain and tenderness and is described as a central augmentation of nociception giving rise to deep tissue tenderness that includes muscles. Studies estimate that in 75–95 percent of cases, myofascial pain is a primary cause of regional pain. Myofascial pain is associated with muscle tenderness that arises from trigger points, focal points of tenderness, a few millimeters in diameter, found at multiple sites in a muscle and the fascia of muscle tissue. Biopsy tests found that trigger points were hyperirritable and electrically active muscle spindles in general muscle tissue.[4]

Qualities of trigger points

Trigger points have a number of qualities. They may be classified as potential, active/latent and also as key/satellites and primary/secondary.

There are a few more than 620 potential trigger points possible in human muscles. These trigger points, when they become active or latent, show up in the same places in muscles in every person. That is, trigger point maps can be made that are accurate for everyone.

An active trigger point is one that actively refers pain either locally or to another location (most trigger points refer pain elsewhere in the body along nerve pathways). A latent trigger point is one that exists, but does not yet refer pain actively, but may do so when pressure or strain is applied to the myoskeletal structure containing the trigger point. Latent trigger points can influence muscle activation patterns, which can result in poorer muscle coordination and balance.Active and latent trigger points are also known as "Yipe" points, for obvious reasons.

A key trigger point is one that has a pain referral pattern along a nerve pathway that activates a latent trigger point on the pathway, or creates it. A satellite trigger point is one which is activated by a key trigger point. Successfully treating the key trigger point often will resolve the satellite and return it from being active to latent, or completely treating it too.

In contrast, a primary trigger point in many cases will biomechanically activate a secondary trigger point in another structure. Treating the primary trigger point does not treat the secondary trigger point.

Activation of trigger points may be caused by a number of factors, including acute or chronic muscle overload, activation by other trigger points (key/satellite, primary/secondary), disease, psychological distress (via systemic inflammation), homeostatic imbalances, direct trauma to the region, accident trauma (such as a car accident which stresses many muscles and causes instant trigger points) radiculopathy, infections and health issues such as smoking.

Trigger points form only in muscles. They form as a local contraction in a small number of muscle fibers in a larger muscle or muscle bundle. These in turn can pull on tendons and ligaments associated with the muscle and can cause pain deep within a joint where there are no muscles. When muscle fibers contract, they use biochemical energy, and these depleted biochemicals become fatigue toxins such as lactic acid. The tightened muscle fibers constrict capillaries and prevent them from carrying off the fatigue toxins to the body's recycling system (liver and kidneys)[citation needed] . The buildup of these toxins in a muscle bundle or muscle feels like a tight muscle -- a slippery elongate bundle.

When trigger points are present in muscles there is often pain and weakness in the associated structures. These pain patterns in muscles follow specific nerve pathways and have been readily mapped to allow for identification of the causative pain factor. Many trigger points have pain patterns that overlap, and some create reciprocal cyclic relationships that need to be treated extensively to remove them.

Diagnosis of trigger points

Trigger points are diagnosed by examining signs, symptoms, pain patterns and manual palpation. Usually there is a taut band in muscles containing trigger points, and a hard nodule can be felt. Often a twitch response can be felt in the muscle by running your finger perpendicular to the muscle's direction; this twitch response often activates the "all or nothing" response in a muscle that causes it to contract. Pressing on an affected muscle can often refer pain. Clusters of trigger points are not uncommon in some of the larger muscles, such as the gluteus group (gluteus maximus, gluteus medius, and gluteus minimus). Often there is a heat differential in the local area of a trigger point, and many practitioners can sense that. In 2007, a paper was presented describing images of trigger points taken by modified MRI.[5]

Misdiagnosis of pain

The misdiagnosis of pain is the most important issue taken up by Travell and Simons. Referred pain from trigger points mimics the symptoms of a very long list of common maladies, but physicians, in weighing all the possible causes for a given condition, rarely consider a myofascial source. The study of trigger points has not historically been part of medical education. Travell and Simons hold that most of the common everyday pain is caused by myofascial trigger points and that ignorance of that basic concept could inevitably lead to false diagnoses and the ultimate failure to deal effectively with pain.[6]

Demonstration and identification of myofascial trigger points

A 2008 review in Archives of Physical Medicine and Rehabilitation of two recent studies concludes they present groundbreaking findings that can reduce some of the controversy surrounding the cause and identification of myofascial trigger points (MTPs). The study by Chen on the use of magnetic resonance elastography (MRE) imaging of the taut band of an MTP in an upper trapezius muscle may open a whole new chapter in the centuries-old search for a convincing demonstration of the cause of MTP symptoms. MRE is a modification of existing magnetic resonance imaging equipment to image stress produced by adjacent tissues with different degrees of tension. This report presents an MRE image of the taut band that shows the chevron-shaped signature of the increased tension compared with surrounding tissues. [7] Results were all consistent with the concept that taut bands are detectable and quantifiable with MRE imaging. The findings in the subjects suggest that the stiffness of the taut bands in patients with myofascial pain may be 50% greater than that of the surrounding muscle tissue. The findings suggest that MRE can quantitate asymmetries in muscle tone that could previously only be identified subjectively by examination.[5]

In the study by Shah and associates, they have shown the feasibility of continuous, in vivo recovery of small molecules from soft tissue without harmful effects. With this technique, they have been able to investigate the biochemical milieu of muscle in subjects with active, latent, or absent myofascial trigger points (MTrPs) and to contrast this with that of the noninvolved muscle. [8]

Dorsher comments on a strong correlation between the locations of trigger points and classical accupuncture points, finding that 92% of the 255 trigger points correspond to accupuncture points, including 79.5% with similar pain indications.[9][10]


Myofascial Trigger Point therapists may use myotherapy (deep pressure as in Bonnie Prudden's approach, massage or tapotement as in Dr. Griner's approach), mechanical vibration, pulsed ultrasound, electrostimulation[11], ischemic compression, injection (see below), dry-needling, "spray-and-stretch" using a cooling (vapocoolant) spray, Low Level Laser Therapy and stretching techniques that invoke reciprocal inhibition within the musculoskeletal system. Practitioners use elbows, feet or various tools to direct pressure directly upon the trigger point, to save their hands.

A successful treatment protocol relies on identifying trigger points, resolving them and, if all trigger points have been deactivated, elongating the structures affected along their natural range of motion and length. In the case of muscles, which is where most treatment occurs, this involves stretching the muscle using combinations of passive, active, active isolated (AIS), muscle energy techniques (MET), and proprioceptive neuromuscular facilitation (PNF) stretching to be effective. Fascia surrounding muscles should also be treated, possibly with myofascial release, to elongate and resolve strain patterns, otherwise muscles will simply be returned to positions where trigger points are likely to re-develop.

The results of manual therapy are related to the skill level of the therapist. If trigger points are pressed too short a time, they may activate or remain active; if pressed too long or hard, they may be irritated or the muscle may be bruised, resulting in pain in the area treated. This bruising may last for a 1–3 days after treatment, and may feel like, but is not similar to, delayed onset muscle soreness (DOMS), the pain felt days after overexerting muscles. Pain is also common after a massage if the practitioner uses pressure on unnoticed latent or active trigger points, or is not skilled in myofascial trigger point therapy.

Evidence based medicine researchers concluded as of 2001 that evidence for the usefulness of trigger points in the diagnosis of fibromyalgia is thin.[12] More recently, an association has been made between fibromyalgia tender points and active trigger points.[13][14]


Injections provide more immediate relief and can be effective when other methods fail. Various injections can be used including saline, local anesthetics such as procaine hydrochloride (Novocain), steroids, and botulinum toxin. Injection with a low concentration, short acting local anesthetic (Procaine 0.5%) without steroids or adrenalin is recommended. High concentrations or long acting local anesthetics as well as epinephrine cause muscle necrosis. Use of steroids can cause tissue damage. Dry needling can be just as effective but causes more post-injection soreness. Botox is rarely indicated.[1]

Despite the concerns about long acting agents[1], a mixture of lidocaine and marcaine is often used.[15] A mixture of 1 part 2% lidocaine with 3 parts 0.5% bupivacaine (trade name:Marcaine) provides 0.5% lidocaine and 0.375% bupivacaine. This has the advantages of immediate anesthesia with lidocaine during injection to minimize injection pain while providing a longer duration of action with a lowered concentration of bupivacaine.

Sarapin can be used for trigger point injection.[16][17] Blue Cross, Medica, HealthPartners and other health insurance companies in the US began covering Trigger Point injections in 2005.


There are a number of ways to self-treat trigger points and these methods are described in numerous texts. Underlying any attempts at self-treatment should be a working knowledge of the area to be treated, especially with regard to the musculature, nerves, glands and vessels.

Trigger points in the male or female pelvis, such as found in chronic pelvic pain syndrome (CPPS), should be treated by physicians trained in the use of intra-rectal trigger point and myofascial release techniques.


Treatment, whether by self or by a professional, has some inherent dangers. It may lead to damage of soft tissue and other organs. The trigger points in the upper quadratus lumborum, for instance, are very close to the kidneys and poorly administered treatment (particularly injections) may lead to kidney damage. Likewise, treating the masseter muscle may damage the salivary glands superficial to this muscle. Furthermore, some experts believe trigger points may develop as a protective measure against unstable joints. 


There are many ideas about how trigger points are formed and why they cause pain. It was once believed that trigger points were scars or inflammation in the muscle. This was disproved when biopsies showed no abnormalities.[citation needed]

More recently it has been proposed that trigger points are spasms or contractures of voluntary muscle, possibly caused by an abnormality at the neuromuscular junction where the nerves controlling muscles connect to the muscle fibers (Travell & Simons). This theory seems unlikely because no contractions of voluntary muscle have been identified by traditional EMG and because the trigger points are often not in the location of the neuromuscular junction.

The most recent proposed mechanism is that trigger points are muscle spindles, made over-active by adrenalin stimulation. These very short muscle fibers, only about 1 cm in length, are called intrafusal muscle fibers to distinguish them from the voluntary muscle fibers which are called extrafusal muscle fibers. Only the intrafusal muscle fibers inside the spindle are activated by adrenalin via the sympathetic nervous system which also controls heart rate, blood pressure and other internal regulatory functions. The “sympathetic spindle spasm” theory of trigger points proposes that when spindles are over-activated by adrenalin they become painful.

The most accepted theory for a trigger point mechanism is that an event of muscular overload causes a prolonged release of Ca2+ ion from the sarcoplasmic reticulum (storage unit for the muscle cell) which results in a sticking of the untrained or overloaded cells. This leads to a contracture with compression of capillaries and results in an increased local energy demand and local ischemia (loss of blood circulation) to the area. This "energy crisis" (as it is termed in the seminal work on trigger points) causes the release of chemicals that augment pain activity. Since an involved muscle is weakened by this theorised sustained shortening, surrounding muscles themselves may develop trigger points in a compensatory fashion.[1][18]

Current hypotheses include:

  • Travell’s Initial Trauma Theory
  • Integrated Trigger Point Hypothesis
  • Pain-Spasm-Pain Cycle
  • Muscle Spindle Hypothesis
  • Neuropathic Hypothesis
  • Fibrotic Scar Tissue Hypothesis

A 2008 review in Arch Phys Med Rehabil. of two recent studies, concludes they present groundbreaking findings that can reduce some of the controversy surrounding myofascial trigger points (MTrPs). The integrated hypothesis is the most credible and most complete proposed etiology of MTrPs. However, the feedback loop suggested in this hypothesis has a few weak links, and studies by Shah and colleagues in particular supply a solid link for one of them. The feedback loop connects the hypothesized energy crisis with the milieu changes responsible for noxious stimulation of local nociceptors that causes the local and referred pain of MTrPs. Shah's reports quantify the presence of not just 1 noxious stimulant but 11 of them with outstanding concentrations of immune system histochemicals. The results also strongly place a solid histochemical base under the important clinical distinction between active and latent MTrPs. [7] Subjects with active MTrPs in the muscle have a biochemical milieu of selected inflammatory mediators, neuropeptides, cytokines, and catecholamines different from subjects with latent or absent MTrPs. [8]


Trigger points have been a subject of study by a small number of doctors for several decades although this has not become part of mainstream medicine. The existence of tender areas and zones of induration in muscles has been recognized in medicine for many years and was described as muscular rheumatism or fibrositis in English; German terms included myogelose and myalgie. However, there was little agreement about what they meant. Important work was carried out by J. H. Kellgren at University College Hospital, London, in the 1930s and, independently, by Michael Gutstein in Berlin and Michael Kelly in Australia (the latter two workers continued to publish into the 1950s and 1960s). Kellgren conducted experiments in which he injected hypertonic saline into healthy volunteers and showed that this gave rise to zones of referred extremity pain.

Today, much treatment of trigger points and their pain complexes are handled by myofascial trigger point therapists, massage therapists, physical therapists, osteopaths, occupational therapists, myotherapists, Certified Athletic Trainer some naturopaths, chiropractors, dentists and acupuncturists, and other hands-on somatic practitioners who have had experience or training in the field of neuromuscular therapy (NMT).

Janet G. Travell, MD

It was, however, an American physician, Janet G. Travell, who was responsible for the most detailed and important work. Her work treating US President John F. Kennedy's back pain was so successful that she was asked to be the first female Personal Physician to the President.[19] She published more than 40 papers between 1942 and 1990 and in 1983 the first volume of The Trigger Point Manual appeared; this was followed by the second volume in 1992. In her later years Travell collaborated extensively with her colleague David Simons. A third edition is soon to be published by Simons and his wife, both of whom have survived Travell.

The trigger point concept remains unknown to most doctors and is not generally taught in medical school curricula. Among physicians, typically only physiatrists (physicians specializing in physical medicine and rehabilitation) are well versed in trigger point diagnosis and therapy. Other health professionals, such as physiotherapists, osteopaths, chiropractors, massage therapists and structural integrators are generally more aware of these ideas and many of them make use of trigger points in their clinical work[20][21].

Travell and Simons' seminal work on the subject, Myofascial Pain and Dysfunction: The Trigger Point Manual[1], states the following:

  • Around 75% of pain clinic patients have a trigger point as the sole source of their pain.
  • Arthritis is often cited as the cause for pain even though pain is not always concomitant with arthritis. The real culprit may be a trigger point, normally activated by a certain activity involving the muscles used in the motion, by chronically bad posture, bad mechanics, repetitive motion, structural deficiencies such as a lower limb length inequality or a small hemipelvis, or nutritional deficiencies.
  • The following conditions are also frequently misdiagnosed as the cause of pain when trigger points are the true cause: carpal tunnel syndrome, bursitis, tendinitis, angina pectoris, and sciatic symptoms, along with many other pain problems.

See also


  1. ^ a b c d e Travell, Janet; Simons David; Simons Lois (1999). Myofascial Pain and Dysfunction: The Trigger Point Manual (2 vol. set, 2nd Ed.). USA: Lippincott Williams & Williams. ISBN 0-683-08363-5. 
  2. ^ a b Tough EA, White AR, Richards S, Campbell J (March–April 2007). "Variability of criteria used to diagnose myofascial trigger point pain syndrome–evidence from a review of the literature". Clin J Pain 23 (3): 278–86. doi:10.1097/AJP.0b013e31802fda7c. PMID 17314589. 
  3. ^ Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz R (Jan 1997). "Interrater reliability in myofascial trigger point examination". Pain 69 (1–2): 65–73. PMID 9060014. 
  4. ^ Jantos M (June 2007). "Understanding chronic pelvic pain". Pelviperineology 26 (2). ISSN 1973–4913. OCLC 263367710.  Full open-access article
  5. ^ a b Chen Q, Bensamoun S, Basford JR, Thompson JM, An KN (December 2007). "Identification and quantification of myofascial taut bands with magnetic resonance elastography". Archives of Physical Medicine and Rehabilitation 88 (12): 1658–61. doi:10.1016/j.apmr.2007.07.020. PMID 18047882. 
  6. ^ Davies Clair, Davies Amber (2004). The trigger point therapy workbook : your self-treatment guide for pain relief (2nd ed.). Oakland, California: New Harbinger Publications. p. 323. ISBN 9781572243750. 
  7. ^ a b Simons DG (2008). "New views of myofascial trigger points: etiology and diagnosis". Archives of Physical Medicine and Rehabilitation 89 (1): 157–9. doi:10.1016/j.apmr.2007.11.016. PMID 18164347. 
  8. ^ a b Shah JP, Danoff JV, Desai MJ, et al. (2008). "Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points". Archives of Physical Medicine and Rehabilitation 89 (1): 16–23. doi:10.1016/j.apmr.2007.10.018. PMID 18164325. 
  9. ^ Dorsher PT (May 2006). "Trigger points and acupuncture points: anatomic and clinical correlations". Medical Accupuncture 17 (3). 
  10. ^ Dorsher PT (July 2009). "Myofascial referred-pain data provide physiologic evidence of acupuncture meridians". J Pain 10 (7): 723–31. PMID 19409857. 
  11. ^ Hsueh TC, Cheng PT, Kuan TS, Hong CZ (November–December 1997). "The immediate effectiveness of electrical nerve stimulation and electrical muscle stimulation on myofascial trigger points". American Journal of Physical Medicine & Rehabilitation 76 (6): 471–6. PMID 9431265. 
  12. ^ "Fibromyalgia: diagnosis and treatment". Bandolier (90). August 2001. ISSN 1353-9906. 
  13. ^ Ge HY, Nie H, Madeleine P, Danneskiold-Samsøe B, Graven-Nielsen T, Arendt-Nielsen L (2009-12-15). "Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome". Pain 147 (1-3): 233–40. PMID 19819074. 
  14. ^ Brezinschek HP (2008 December). "[Mechanisms of muscle pain : significance of trigger points and tender points]" (in German). Z Rheumatol 67 (8): 653–4, 656-7. doi:10.1007/s00393-008-0353-y. PMID 19015861. 
  15. ^ "Trigger point injection". Non-Surgical Orthopaedic & Spine Center. October 2006. Retrieved 2007-04-07. 
  16. ^ "Sarapin: A regional Analgesic for control of pain of neuralgic origin.". Retrieved 2007-04-03. 
  17. ^ "PDR entry for Sarapin". Retrieved 2007-04-03. 
  18. ^ Simons DG (2003). "Cardiology and myofascial trigger points: Janet G. Travell's Contribution". Tex Heart Inst J 30 (1): 3–7. PMID 12638663. 
  19. ^ Bagg JE (2003). "The President's physician". Tex Heart Inst J 30 (1): 1–2. PMID 12638662. 
  20. ^ Alvarez DJ, Rockwell PG (February 2002). "Trigger points: diagnosis and management". Am Fam Physician 65 (4): 653–60. PMID 11871683. 
  21. ^ Dynamic Chiropractic

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