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.
Trigger point myalgia can occur in every age range, elderly people are more proposed for trigger point myalgia do to several factors as prolonged paramorphistic postures, autoimmune syndromes, biochemical structure changes, injuries etc. etc.
The evolution of non treated trigger point leads to progressive fibrosis in the tissue and could manifest into Miofascial Pain Syndrome.
Prognosis is non favorable for about 5% of patients affected, who inevitably will manifest cronic persistent pain.
Trigger points have a number of qualities. They may be classified as active/latent and also as key/satellites and primary/secondary.
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.
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, psycho-emotional disorders, homeostatic imbalances, direct trauma to the region, radiculopathy, infections and health choices such as smoking.
Trigger points can appear in many myofascial structures including muscles, tendons, ligaments, skin, joint capsule, periosteal, and scar tissue. When 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.
Local intermittent irritant burning sensation or local and irradiating pain in specific areas. 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.
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.
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, intrafusal muscle fibers, made over-active by adrenalin stimulation. 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. This theory supports the idea that stress and decrease of moderate physical activity in modern lives has increased the occurrence of myofascial pain and trigger points.
Another idea 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 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.
Both the above are accepted to be true and the integrated hypothesis is the most credible and most complete proposed etiology of Trigger Point syndrome.
The hypothesized energy crisis with the milieu changes responsible for noxious stimulation of local nociceptors that causes the local and referred pain could be caused by an outstanding concentrations of immune system histochemicals.
Current hypotheses even include: Travell’s Initial Trauma Theory, Integrated Trigger Point Hypothesis, Pain-Spasm-Pain Cycle, Muscle Spindle Hypothesis, Neuropathic Hypothesis, Fibrotic Scar Tissue Hypothesis.
Diagnosis of trigger points is 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.
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, have rarely even conceived of there being 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.
A 2008 review in Archives of Physical Medicine and Rehabilitation of two recent studies with the use of magnetic resonance elastography (MRE is a modification of existing magnetic resonance imaging equipment to image stress produced by adjacent tissues with different degrees of tension.) Imaging of the taut band of an MTP in an upper trapezius muscle shows the chevron signature of the increased tension compared with surrounding tissues.
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.
Prior to treatment commencement, the therapist should be sure be that the pain patterns they are treating lend themselves to
Trigger Point Therapy. If the patient presents with swelling, discoloration, or neurological symptoms, it is always advisable to refer to another health/medical care provider regarding further examination and/or investigation.
Treatment of trigger points may be by manual, Myofascial Trigger Point Therapy by a trained Myofascial Trigger Point Therapist, Myotherapy (deep pressure as in Bonnie Prudden's approach, massage or tapotement as in Dr. Griner's approach), mechanical vibration, pulsed ultrasound, electrostimulation, ischemic compression, injection (see below), dry-needling, "spray-and-stretch" using a cooling (vapocoolant) spray, and stretching techniques that invoke reciprocal inhibition within the musculoskeletal system.
Use of elbows, feet or various tools to direct pressure directly upon the trigger point often occurs, to save practitioner's 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.
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 Botox. 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 skin atrophy. Dry needling (like local acupuncture) can be just as effective but causes more post-injection soreness. Botox is rarely indicated.
Despite the concerns about long acting agente, a mixture of lidocaine and Bupivicaine is often used. A mixture of 1 part 2% lidocaine with 3 parts 0.5% Bupivicaine provides 0.5% lidocaine and 0.375% Bupivicaine. 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 Bupivicaine. Sarapin can be used to for trigger point injection.
parameters Bupivacaina 0,5% Anesthetic + cortisone Agopuntura Stretch + spray
TPs injected 300 310 210 30
TPs extinguished 245 243 121 2
TPs extinguished 81 78 57 -
Treated patients 132 132 151 11
Heald patients 121 122 98 Not known Healness 91 92 60 -
Tabel 3 – Effectiveness confrontation among various trigger point techniques
There are a number of ways to self-treat trigger points and these methods are described in numerous texts. Due to the controversy related to this field, as well as its relative newness, no single guide should be taken as the sole or final truth. 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.
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 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, some osteopaths, 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 was, however, an American physician, 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. 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 myofascial trigger point therapists, physiotherapists, naturopaths, chiropractors, dentists, massage therapists and structural integrators and some veterinarians are generally more aware of these ideas and many of them make use of trigger points in their clinical work.
Travell and Simon's seminal work on the subject, “Myofascial Pain and Dysfunction”: The Trigger Point Manual, 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.