Myofascial “trigger points”, coined in the 1950’s by Dr. Janet Travell and Dr. David Simon, are commonly defined in clinical practice as the presence of deep local tenderness at a nodule in a palpable taut band of muscle which, when stimulated, can cause a referred pattern of pain. Trigger points can produce referred pain to other musculature spontaneously or with manual compression to the site within the muscle. Myofascial trigger points can present in individuals through occupational or athletic activities, where postural deficiencies, muscle imbalances, and overuse injuries can occur.

Anatomy of Myofascial Trigger Points

Voluntary muscle contraction is controlled by the central nervous system. Motor centers in the brain sends signals, in the form of action potentials, to anterior horn alpha motor neurons that innervate extrafusal muscle fibers. Contraction of muscle fibers occurs when the neurotransmitter acetylcholine is released into the neuromuscular junction from presynaptic clefts and binds to receptors on the muscle cell membrane at the motor end plate zone. The binding of acetylcholine causes calcium to enter the muscle cell. As a result of calcium troponin proteins move the myosin heads up the actin molecule. This flow of events causes the sarcomere, the functional unit of the muscle, to shorten and contract.¹ (figure 1)
Figure 1.JPG
Trigger points (TrPs) are located at the center, or belly, of the muscle in the motor endplate zone. Motor nerves in this zone enter a muscle and divide into branches each with a terminal claw-like motor endplate embedded in the surface of a muscle fiber. Muscle fibers with active TrPs contract to form a distinctive taut band. Normal muscle fibers have sarcomeres of equal length. Muscle fibers containing contraction knots, or “fusiform swellings”, have shortened sarcomeres at the site and lengthened muscle fibers on either side. (figure 2) Neurovascular bundles associated with TrP sites contain a motor axon with branching motor nerve endings that have terminal motor endplates with contractile “knots”. Nociceptive and proprioceptive sensory afferents, blood vessels, and associated sympathetic fibers are also found within the bundle.²

Trigger Point Pathophysiology

Figure 2.JPGTrigger points can be found in skin and periosteum but are most prevalent in muscle tissue. There are several theories surrounding the underlying causes of Tp’s. One of the widely excepted mechanisms is the Motor Endplate Hypothesis which identifies dysfunction in the region of extrafusal motor endplates as a primary cause of myofascial TrPs.³ It is suspected that when pain develops at the site of a TrP, sensitized nociceptor sensory afferents release calcitonin gene-related peptides which then cause an increased rate of release of acetylcholine from motor endplates further contracting muscle fibers.⁴
Though skepticism still surrounds this mechanism of Tp formation, electromyography (EMG) studies have demonstrated that spontaneous electrical activity found at TrP sites correspond to abnormal patterns of motor end plate electrical activity brought about by excessive release of acetylcholine. Trigger points cannot be seen on X-ray; however they have been viewed with electron microscopy in fresh human cadavers.

Nociceptor Activity and Myofascial Trigger Points

Heightened sensitivity of group C (nonmylinated) nociceptors is responsible for the acute pain of myofascial TrP’s. Nociceptors are free (bare) nerve ending sensory receptors that detect signals from damaged tissue. Nociceptors are found in the skin, muscle, joints, bone and viscera. (figure 3)

The cell bodies of nociceptors are mainly in the dorsal root and trigeminal ganglia. Pain signals from nociceptors are sent to the central nervous systems via the neospinothalamic pathway, or simply the spinothalamic pathway. (figure 4-blue)
Pathway details:
1.The central processes of nociceptors enter the dorsal horn of the spinal cord in the dorsolateral fasiculus of Lissauer.
2.First order fibers ascend approximately two levels before synapsing on second-order neurons in lamina of Rexed regions I,II,V.
3.Second order neurons decussate across the anterior comissure and ascend in the contralateral lateral spinothalamic tract.
4.These fibers will ascend through the medulla and through the pons and midbrain as the spinal lemniscus until synapsing in the Ventroposteriorlateral (VPL) nucleus of the thalamus.
5.The third order neurons in the thalamus project through the internal capsule and corona radiata to the main somatosensory cortex SI, Brodmann's Areas 3, 1, and 2.

Figure 3.JPGfigure 4.JPG

Sensory symptoms related to myofascial trigger points can range from local and referred pain in the form of a widespread muscle aches worsened with movement, to muscle stiffness, weakness, edema, nausea, and postural distortions. Nociceptor sensitivity in skeletal muscle fibers can be caused by several factors, the most common being muscle trauma from overload, injury, or microtrauma in the form of repetitive strain injuries. Anxiety can induce Tp formation in stressed individuals that hold specific muscles in prolonged states of contraction (bracing). It is believed that TrP’s form in these muscles due to sympathetic nerve over-activity, or the over stimulation of parallel axons for pain and motor control pathways in the reticulospinal tract. Compression or entrapment of motor nerves, muscle ischemia and wasting due to neurological pathology, and environmental conditions can also play a role in nociceptor sensitivity.Trigger points can be identified when firm pressure is applied to the muscle tissue above the TrP site inducing a “jump sign”, an involuntarily reflexive withdrawal movement of the limb from the response to pain.

Types of Trigger Points

There are four classifications of trigger points: primary, secondary, satellite, and latent. Primary TrP’s contain nociceptor activity in the center of a muscle, or a group of muscles, and is mainly responsible for the development of the myofascial pain. Secondary TrP’s develop in synergistic muscles of the affected muscle. An imbalance of tension in the primary muscle, due to shortening muscle fibers, and compensatory overload of the synergistic muscles causes secondary Tp sites to develop. A satellite Tp forms within the pain referral zone of another muscle containing a primary Tp. According to Davies and Davies ‘long term chronic pain is often a compound effect from a chain of satellite trigger points, cascading from muscle to muscle.’ Satellite Tp’s can sometimes resolve independently if the primary Tp site is deactivated. Secondary Tp’s can also form at muscle attachment sites in highly sensitized connective tissue. A Latent Tp is a site where nociceptors have become active but not sensitized enough to cause pain. However, these areas are painful and produce a ‘jump sign’ when the tissue is compressed above the latent site.

Pain Referral

Pain referral from myofascial trigger points has not been shown to follow a nerve root distribution pattern.⁸ Many theories have been investigated to understand the mechanisms that underlie pain referral from myofascial Tp’s. One idea is the hypothesis of convergence which argues that information transmitted centripetally from dorsal horn convergent neurons (sensory and muscle afferents) is not specific enough for the brain to distinguish between various input sources to the spinal cord. Another study cites neuroplastic changes of the receptive field size and number of sensory inputs from muscle nociceptors as a plausable answer, but reliable and clinically significant studies have yet to emerge. ²

Janet Travell M.D (1901-1997) was a pioneer in developing techniques for myofascial pain. Together with co-author David G. Simons, they wrote the acclaimed Myofascial Pain and Dysfunction: the Trigger Point Manual, a widely used resource for manual and physical therapists. Travell’s great discovery was that referred pain occurs in very predictable patterns in everyone, with only small variations. She notes that “referred pain seems to occur in or near a joint, where pain would most likely make a person modify the activity that may have created the problem; an evolutionary advantage.” ⁶ The book features topographical maps of trigger point patterns and referral zones in detail, including treatment protocols for the practitioner. (figure 5)
figure 5.JPG
At the present time there are no reliable laboratory or imaging tests currently available for making the diagnosis of myofascial TrPs. At most a thorough health history should be performed to identify the clinical features of TrP’s. Clinical features used as primary indicators in lieu of diagnostic methods include palpable nodules, or taut bands in muscles that elicit the ‘jump sign’, local twitch responses, and referred pain and tenderness.

Treatment Methods

The persistence of trigger points has remained a frustration for many patients and practitioners. Trigger points may be successfully deactivated only to return after successful treatments. There may be many explanations for why Tp’s persist in individuals, including physical factors such as postural stress, repetitive movement patterns related to occupational activities, vitamin and mineral deficiencies, and psychological factors such as stress, tension and anxiety. Spinal dorsal horn plasticity and self-perpetuating circuits between Tp’s and the spinal cord motor efferent activity (reflex pain arc), may also help to explain Tp recurrence.

Practitioners certified in Manual Trigger Point Therapy, including physicians, physical therapists, massage therapists, nurses and other licensed healthcare professionals receive specialized training in the identification, treatment and elimination myofascial Tp pain. The Trigger Point Manual by Travell and Simons covers several treatment methods in comprehensive detail: trigger point injection, spray and stretch, and massage techniques.
Trigger Point Injection
Trigger points are injected with a local anesthetic. The needle mechanically disrupts the Tp’s contracted muscle fibers and the anesthetic decreases pain at the site. Injections appear to be the quickest treatment for new Tp formation, with chronic Tp sites requiring multiple, and frequent, injections. Skill and precision is required for injections as procedural errors can result in injury to healthy tissue.

Trigger Point Dry Needling
A similar method, called dry needling, is used by physical therapist and physicians but without the anesthetic. A needle is inserted through the skin and muscle directly into the Tp producing a local twitch response, an involuntary spinal cord reflex in which the muscle fibers in the taut band of muscle contracts. The twitch response indicates the proper placement of the needle in the Tp. Studies have shown that dry needling mechanically disrupts the integrity of the dysfunctional endplates within the trigger area causing a mechanical and physiological resolution of the TrPs.⁹ The principle behind dry needling is the reflex arc; pain signals return through sympathetic ganglion and activate primary afferent nocioceptors which feed back to the spinal cord. In parallel, motor neurons become stuck in a feedback loop, facilitating muscle spasms. In dry needling the needle impedes the reflex arc relaxing the muscle. ¹⁰(figure 6).
Figure 6.JPG

Spray and Stretchfigure 7.JPG
Skin at the site of the Tp is sprayed with a refrigerant followed by stretching the affected muscle.
This method requires less skill then the injection, however stretching only the muscle that is
referring the Tp is key, as well as working quickly with the cooling agent, and rewarming the skin.
Chilling the skin prevents defensive tightening of the muscle by temporarily distracting the nervous
system and suppressing pain.

According to Travell and Simons the safest and most effective method of trigger point therapy is deep
massage applied directly to the trigger point. This treatment is more direct, carries less risk, and for some
an effective self-treatment. Deep stroking massage across a trigger point nodule moves blood and lymph
through the contracted tissue and brings elasticity back to the muscle fibers. Pain is intermittent with this
technique making it an easy, non-invasive treatment method to tolerate.


A recent market research report in 2011 indicates that more than 1.5 billion people worldwide suffer from chronic pain and that approximately 3- 4.5% of the global population suffers from neuropathic pain, with incidence increasing with age.¹¹ In regards to the four most common types of pain, respondents of a National Institute of Health Statistics survey indicated that low back pain was the most common (27%), followed by severe headache or migraine pain (15%), neck pain (15%) and facial ache or pain (4%).¹²

Travell and Simon believe that myofascial trigger point syndrome is the primary cause of musculoskeletal pain experienced by the general public, and is often misdiagnosed, and treated ineffectively by health care practitioners without proper training or awareness. As medical science progresses to create diagnostic tools for identifying the causes of myofascial pain, chronic pain continues to dominate society. Examining the musculoskeletal system as a whole and exploring new ways of treating chronic problems will increase awareness of myofascial trigger point syndromes and new paradigms of patient care will emerge.


Trigger point – hyperirritable spots in skeletal muscle that are associated with palpable nodules in taut bands of muscle fibers.
Neuromuscular junction – connects the nervous system to the muscular system via synapses between efferent nerve fibers and muscle fibers, also known as muscle cells.
Nociceptor – sensory receptors that responds to potentially damaging stimuli by sending nerve signals to the spinal cord and brain.
Sarcomere – the basic unit of a muscle. Sarcomeres are composed of long, fibrous proteins that slide past each other when muscles contract and relax.
Troponin - attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue.
Actin – a globular, multi-functional protein in muscle tissue that forms the thin element where myosin binds.
Myosin - ATP-dependent motor proteins in muscle tissue that forms the thick filament and binds to actin. Myosins binding to actin forms cross bridges for the contraction of muscle to begin.


1) The Motor Endplate Hypothesis finds the decreased release of acetylcholine the primary cause of myofascial trigger point formation.
2) Pain from trigger points can be referred to adjacent musculature but does not follow a nerve root distribution pattern.
3) Sensory information for pain ascends to the CNS via the medial limniscal pathway.
4) Trigger points are only found in muscle.
5) A Latent trigger point is a site where nociceptors have become active but not sensitized enough to cause pain.
6) Massage is an effective and safe non-invasive means of deactivating trigger points.
7) Dry needling mechanically disrupts the integrity of muscle fibers and is not an effective means of treatment for trigger point resolution.

Multiple Choice

1. Satellite trigger point is defined as:
A. a site where nociceptors have become active but not sensitized enough to cause pain
B. a site that contains nociceptor activity in the center of a muscle
C. trigger point formation within the pain referral zone of another muscle containing the primary trigger point

2. Trigger point treatment methods do not include which of the following
A. ballistic muscle stretching
B. spray and stretch
C. massage

3. All of the following are clinical features of myofascial trigger points except:
A. taut bands in muscles
B. x-ray image of nodule in muscle
C. referred pain and tenderness
D. local twitch response

T/F Answers [F,T,F,F,T,T,F]
Multiple Choice Answers [C, A, B]

Further Resources is an excellent reference for pain patterns and trigger point diagrams. For additional information on trigger points and some very informative articles.
The NAMTPT is a professional organization dedicated increasing the public awareness of and access to myofascial pain treatment. They serve the professionals who recognize and treat myofascial trigger points by offering member resources and continuing education.

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Figure 1: (accessed 12/15/12)
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Figure 4: figure 6.1 (accessed 12/15/12)
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Figure 7: spray and stretch (accessed 12/15/12)
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