Concept:Trigger Point
General Overview of Myofascial Trigger Points
A. Background
Prevalence
Myofascial trigger points (TrPs) are extremely common and become a painful part of nearly everyone's life at some time or another. Latent TrPs, which often cause motor dysfunction (stiffness and restricted range of motion) without pain, are far more common than active TrPs, which additionally cause pain.
Among 200 unselected asymptomatic young adults, focal tenderness representing latent TrPs was found in the shoulder-girdle muscles of 54% of females and 45% of males. Referred pain was demonstrated in 25% of these subjects. In masticatory muscles, TrPs were found in 54% of right lateral pterygoid muscles, 45% of right deep masseter, 43% of right anterior temporalis, and 40% of intraoral examinations of the right medial pterygoid muscle. In the neck muscles, TrPs were identified in 35% of the right splenius capitis and 33% of the right upper trapezius.
| Region | Practice | Number Studied | % with Myofascial Pain | Source |
|---|---|---|---|---|
| General | Medical | 172 (54) | 30% | Skootsky et al., 1989 |
| General | Pain Med. Center | 96 | 93% | Gerwin, 1995 |
| General | Comprehensive Pain Center | 283 | 85% | Fishbain et al., 1986 |
| Craniofacial | Head & Neck Pain Clinic | 164 | 55% | Fricton et al., 1985 |
| Lumbogluteal | Orthopedic Clinic | 97 | 21% | Fröhlich and Fröhlich, 1995 |
Among 283 consecutive admissions to a comprehensive pain center, a primary organic diagnosis of myofascial syndrome was assigned in 85% of cases. Active myofascial TrPs are clearly very common and are a major source of musculoskeletal pain and dysfunction, but poor agreement on appropriate diagnostic criteria has been a serious handicap to wider recognition.
Importance
Voluntary (skeletal) muscle is the largest single organ of the human body, accounting for nearly 50% of body weight. The Nomina Anatomica lists 200 paired muscles, totalling 400 muscles. Any one of these muscles can develop myofascial TrPs that refer pain and motor dysfunction, often to another location.
The severity of symptoms caused by myofascial TrPs ranges from agonising incapacitating pain caused by very active TrPs to the painless restriction of movement and distortion of posture due to latent TrPs. The economic cost is incalculable. Unrecognised myofascial headache, shoulder pain, and low back pain have become chronic major causes of industrial lost time and compensation applications. Active TrPs in their mature years of maximum activity are most likely to afflict individuals; with advancing age, latent TrPs tend to become more prominent than the pain of active TrPs.
Severity ranges from agonising incapacitation to the painless restriction of movement. Patients in a general medicine practice rated their pain as high as, or higher than, pain due to other causes. Patients who have had other kinds of severe pain — such as that due to a heart attack, broken bones, or renal colic — say that myofascial pain from TrPs can be just as severe.
Historical Review
The history of identifying specific sources of musculoskeletal pain has been slow and spotty.
| Term Used | Muscular Findings | Author, Year |
|---|---|---|
| Muskelschwiele [Muscle callus] | Tender tight cord or band | Froriep, 1843 |
| Muscular rheumatism | Tender, elongated infiltrations, radiating pain | Adler, 1900 |
| Fibrositis | Tender fibrous beaded chains | Gowers, 1904 |
| Fibrositis / Myofibrositis | Tender nodules with radiating pain | Llewellyn & Jones, 1915 |
| Myogelose [muscle gelling] | Tender muscle indurations (persisted after death) | Schade, 1919 |
| Muskelhärten [muscular indurations] | Tender indurations with or without muscular contraction | F. Lange, 1925 |
| Muskelhärten, Myogelosen | The first "trigger point manual;" referred pain not mentioned | M. Lange, 1931 |
| Muskelhärten | Introduction of ethyl chloride spray | Kraus, 1937 |
| Referred pain | Experimental demonstration of pain referred from muscle | Kellgren, 1938 |
| Idiopathic myalgia | Spot tenderness, referred pain, decreased ROM (first description of TrPs) | Travell et al., 1942 |
| Myofascial TrPs | Tender spot, referred pain, 32 pain patterns | Travell R., 1952 |
| Trigger Areas | Electromyographic activity of trigger areas first reported | Weeks & Travell, 1957 |
| Fibromyalgia | Renamed the 1977 redefinition of fibrositis | Yunus et al., 1981 |
| Myofascial TrP | Publication of Volume 1 of the Trigger Point Manual | Travell & Simons, 1983 |
| Myofascial TrPs | Needle EMG activity characteristic of TrPs reported | Hubbard & Berkoff, 1993 |
| Active Loci | Use of the rabbit as an experimental model to study the electrical activity of TrPs | Simons et al., 1995 |
| Myofascial TrPs | New research data for selection of diagnostic criteria; experimental basis for the new dysfunctional endplate hypothesis | Simons, 1996 |
| Myofascial TrPs | Interrater reliability; identified TrP diagnostic criteria | Gerwin et al., 1997 |
Three clinicians on three continents simultaneously and independently published papers in English emphasising four cardinal features of tender muscle spots: a palpable nodular or band-like hardness in the muscle, a highly localised spot of extreme tenderness in that band, reproduction of the patient's distant pain complaint by digital pressure on that spot, and relief of the pain by massage or injection of the tender spot.
Michael Gutstein (published as Gut-stein, Gutstein-Good, and finally Good from Great Britain) published 12 or more papers in Britain between 1938 and 1957 using terms including myalgia, idiopathic myalgia, and nonarticular rheumatism.
Michael Kelly (Australia) published nearly a dozen papers on "fibrositis" between 1941 and 1963, was impressed by both the palpable hardness of the nodule and the distant referral of pain from the afflicted muscle.
Janet Travell (United States) published more than 40 papers between 1942 and 1990, and the first volume of The Trigger Point Manual was published in 1983. She reported the pain patterns of TrPs in 32 skeletal muscles. It was her opinion that any fibroblastic proliferation was secondary to a local muscular dysfunction and that pathologic changes occurred only after the condition continued for a long time.
By 1990, rheumatologists under the leadership of F. Wolfe officially established diagnostic criteria for fibromyalgia. Since then, remarkable progress has been made toward identifying its cause — it is now firmly established that central nervous system dysfunction is primarily responsible for the increased pain sensitivity of fibromyalgia.
An important milestone was reached by Hubbard and Berkoff in 1993 when they convincingly reported needle EMG activity characteristic of myofascial TrPs. In 1994, Hong and Torigoe demonstrated that the rabbit was a suitable experimental model for studying the LTR. In 1995, Simons et al. confirmed in rabbit experiments the electrical activity reported by Hubbard and Berkoff.
Related Diagnostic Terms
The cause of muscle pain syndromes has perplexed the medical community for more than a century. The subject has been plagued by a multitude of overlapping terms:
- Fibromyalgia — fundamentally a different condition from myofascial TrPs but often presents with confusingly similar symptoms. Characterised by central augmentation of nociception, causing generalised deep tissue tenderness that includes muscles. Different etiology, different treatment.
- Fibrositis — appeared in English literature in 1904; adopted into German as Fibrositissyndrom. Used the palpable "fibrositic" nodule as a diagnostic criterion. In 1977, Smythe and Moldofsky completely redefined the condition and it was officially established as fibromyalgia in 1990. Fibrositis is currently an outmoded diagnosis.
- Muskelhärten (literally "muscle hardenings" or "indurations") — the palpable firmness of the tender nodule responsible for the patient's pain.
- Myogelose (literally "muscle gellings") — refers to the same phenomena as Muskelhärten; the two terms have frequently been used interchangeably.
- Myofascial Pain Syndrome — has both a general meaning (any regional muscle pain syndrome of any soft tissue origin associated with muscle tenderness) and a specific meaning (a myofascial pain syndrome caused by TrPs, which is the subject of this book). The unmodified, unspecified use of the term is discouraged.
- Myofascitis — now rarely (and should not be) used synonymously with myofascial TrPs. Properly used to identify inflamed muscles.
- Nonarticular Rheumatism — a commonly used but not clearly defined general term for soft tissue pain syndromes not associated with a specific joint dysfunction or disease. Currently used synonymously with soft tissue rheumatism (Weichteilrheumatismus).
- Osteochondrosis — used by Russian vertebroneurologists as an inclusive term to cover the interaction of neural and muscular conditions, such as fibromyalgia, myofascial TrPs, and spinal nerve compromise.
- Tendomyopathy — English version of the German term. General tendomyopathy is considered synonymous with fibromyalgia; the localised form often includes myofascial TrPs.
B. Clinical Characteristics of Trigger Points
Symptoms
Active TrPs produce a clinical complaint (usually pain) that the patient recognises when the TrP is digitally compressed. Latent TrPs can produce the other effects characteristic of a TrP — including increased muscle tension and muscle shortening — but do not produce spontaneous pain. Both active and latent TrPs can cause significant motor dysfunction. An active key TrP in one muscle can induce an active satellite TrP in another muscle. Inactivation of the key TrP often also inactivates its satellite TrP without treatment of the satellite TrP itself.
Onset. The activation of a TrP is usually associated with some degree of mechanical abuse of the muscle in the form of muscle overload, which may be acute, sustained, and/or repetitive. Leaving the muscle in a shortened position can convert a latent TrP to an active TrP — this process is greatly aggravated if the muscle is contracted while in the shortened position. In paraspinal (and very likely other) muscles, a degree of nerve compression that causes identifiable neuropathic electromyographic changes is associated with an increase in the number of active TrPs.
Pain Complaint. Patients with active myofascial TrPs usually complain of poorly localised, regional, aching pain in subcutaneous tissues, including muscles and joints. They rarely complain of sharp, clearly-localised cutaneous-type pain. The myofascial pain is often referred to a distance from the TrP in a pattern that is characteristic for each muscle. Sometimes the patient is aware of numbness or paraesthesia rather than pain.
Active TrPs are found commonly in postural muscles of the neck, shoulder and pelvic girdles, and in the masticatory muscles. In addition, the upper trapezius, scalene, sternocleidomastoid, levator scapulae, and quadratus lumborum muscles are very commonly involved.
The intensity and extent of the referred pain pattern depends on the degree of irritability of the TrP, not on the size of the muscle.
Dysfunctions. In addition to the clinical symptoms produced by the sensory disturbances of referred pain, dysaesthesias, and hyperaesthesias, patients can also experience clinically important disturbances of autonomic and motor functions.
Disturbances of autonomic functions caused by TrPs include abnormal sweating, persistent lacrimation, persistent coryza, excessive salivation, and pilomotor activities. Related proprioceptive disturbances include imbalance, dizziness, tinnitus, and distorted weight perception of lifted objects.
Disturbances of motor functions caused by TrPs include spasm of other muscles, weakness of the involved muscle function, loss of coordination by the involved muscle, and decreased work tolerance of the involved muscle. The weakness and loss of work tolerance are often interpreted as an indication for increased exercise, but if this is attempted without inactivating the responsible TrPs, the exercise is likely to encourage and further ingrain substitution by other muscles.
Sleep Disturbances. Disturbance of sleep can be a problem for patients with a painful TrP syndrome. Sleep disturbance can, in turn, increase pain sensitivity the next day.
Physical Findings
A muscle harbouring a TrP is prevented by pain from reaching its full stretch range of motion, and is also restricted in its strength and/or endurance. Clinically, the TrP is identified as a localised spot of tenderness in a nodule in a palpable taut band of muscle fibres.
Taut Band. By gently rubbing across the direction of the muscle fibres of a superficial muscle, the examiner can feel a nodule at the TrP and a rope-like induration that extends from this nodule to the attachment of the taut muscle fibres at each end of the muscle. The taut band can be snapped or rolled under the finger in accessible muscles. With effective inactivation of the TrP, this palpable sign becomes less tense and often (but not always) disappears.
Tender Nodule. Palpation along the taut band reveals a nodule exhibiting a highly localised, exquisitely tender spot that is characteristic of a TrP.
Recognition. Application of digital pressure on either an active or latent TrP can elicit a referred pain pattern characteristic of that muscle. However, if the patient recognises the elicited sensation as a familiar experience, this establishes the TrP as being active and is one of the most important diagnostic criteria available when the palpable findings are also present. Similar recognition is frequently observed when a needle penetrates the TrP and encounters an active locus.
Referred Sensory Signs. In addition to referring pain to the reference zone, TrPs may refer other sensory changes such as tenderness and dysaesthesias.
Local Twitch Response (LTR). Snapping palpation of the TrP frequently evokes a transient twitch response of the taut band fibres. This is fully described in Section D of this chapter. The LTR can be elicited both from active and latent TrPs.
Limited Range of Motion. Muscles with active myofascial TrPs have a restricted passive (stretch) range of motion because of pain. An attempt to passively stretch the muscle beyond this limit produces increasingly severe pain because the involved muscle fibres are already under substantially increased tension at rest length.
Painful Contraction. When a muscle with an active TrP is strongly contracted against fixed resistance, the patient feels pain. This effect is most marked when an attempt is made to contract the muscle in a shortened position.
Weakness. Although weakness is generally characteristic of a muscle with active myofascial TrPs, the magnitude is variable. EMG studies indicate that, in muscles with active TrPs, the muscle starts out fatigued, fatigues more rapidly, and becomes exhausted sooner than normal muscles.
Testing
No laboratory test or imaging technique has been generally established as diagnostic of TrPs. However, three measurable phenomena help to substantiate objectively the characteristic TrP phenomena, and all are valuable as research tools:
Needle Electromyography (EMG). In 1993, Hubbard and Berkoff reported finding EMG activity identified as specific to myofascial TrPs — specifically the presence of spontaneous low-voltage motor endplate "noise" activity as well as high-voltage spike activity. Subsequent rabbit and human studies have confirmed the presence of these two distinctive components. This is considered highly characteristic of myofascial TrPs, though not pathognomonic. The source of the high-voltage spikes can be ambiguous. A detailed consideration of this phenomenon appears in Section D of this chapter.
Ultrasound Imaging. Visualisation of an LTR using ultrasound was first noted by Michael Margolis, M.D., and was followed up by Gerwin and Duranleau. This imaging procedure not only provides a second way, in addition to EMG recording, of substantiating and studying the LTR, but also has strong potential for providing a much-needed, available imaging technique to objectively substantiate the clinical diagnosis of TrPs.
Surface Electromyography (sEMG). Trigger points cause distortion or disruption of normal muscle function. A muscle with a TrP exhibits a three-fold problem: increased responsiveness, delayed relaxation, and accelerated fatigability, which together increase overload and reduce work tolerance.
- Increased responsiveness — abnormally high amplitude of EMG activity when the muscle is voluntarily contracted and loaded.
- Accelerated fatigability' — reduced work tolerance compared to a normal contralateral muscle. EMG amplitude increases and median power frequency decreases significantly.
- Delayed relaxation' — failure to relax; a common finding during repetitive exercises of muscles with myofascial TrPs. Loss of normal brief surface EMG gaps during repetitive movements contributes significantly to muscle fatigue.
Algometry. Sensitivity to pain has been measured as the pain threshold to applied pressure. Three endpoints are reported: onset of local pain (pressure pain threshold), onset of referred pain (referred pain threshold), and intolerable pressure (pain tolerance). A hand-held spring algometer is widely used in research. However, tenderness by itself cannot serve as a diagnostic criterion because it may be due to myofascial TrPs, fibromyalgia tender points, bursitis, severe spasm, etc.
Thermography. Thermograms can demonstrate cutaneous reflex phenomena characteristic of myofascial TrPs. The undisturbed TrP may tend to induce hyperthermia in a limited area of the skin overlying the TrP, whereas mechanical stimulation of the TrP induces a reflex hypothermia. However, thermographic evidence is not sufficient alone to identify a TrP, as similar temperature changes can occur from radiculopathy, articular dysfunction, enthesopathy, or local subcutaneous inflammation.
Treatment
Effective treatment of a myofascial pain syndrome caused by TrPs usually involves more than simply applying a procedure to the TrPs. It is often necessary to consider and deal with the cause that activated the TrPs, to identify and correct any perpetuating factors (which are often different from what activated the TrPs), and to help the patient restore and maintain normal muscle function.
Treatment approaches include the use of simple muscle stretch, augmented muscle stretch, postisometric relaxation, reciprocal inhibition, slow exhalation, eye movement, TrP pressure release, massage, range of motion, heat, ultrasound, high-voltage galvanic stimulation, drug treatment, biofeedback, and injection techniques.
Common Misconceptions About Treatment:
- Simply treating the TrP should be sufficient — this is occasionally true IF the stress that activated the TrP is not recurrent and IF there are no perpetuating factors. Otherwise, the TrP is likely to be reactivated by the same stress.
- The pain cannot be as severe as the patient says and must be largely psychogenic — the patients are trying to communicate their suffering. Believe them. The pain rates as fully as severe as that of rheumatoid arthritis.
- Myofascial pain syndromes are self-limiting and will cure themselves — an acute uncomplicated TrP activated by an unusual activity or muscle overload can revert spontaneously to a latent TrP within a week or two, IF the muscle is not over-stressed and IF there are no perpetuating factors. Otherwise, it evolves into a chronic myofascial pain syndrome.
- Relief of pain by treatment of skeletal muscles for myofascial TrPs rules out serious visceral disease — because of the referred pain nature of visceral pain, application of vapocoolant spray or infiltration of a local anaesthetic into the somatic reference zone can temporarily relieve the pain of myocardial infarction, angina, and acute abdominal disease.
Diagnostic Criteria
The lack of general agreement as to appropriate diagnostic criteria for examining TrPs has been an increasingly serious impediment to wider recognition of myofascial TrPs and to compatible studies of the effectiveness of treatment.
| Examination | Mean Kappa | Difficulty | Diagnostic Value Alone |
|---|---|---|---|
| Spot Tenderness | 0.70 | + | +* |
| Pain Recognition | 0.59 | ++ | +++ |
| Palpable Band | 0.54 | +++ | ++* |
| Referred Pain | 0.47 | +++ | + |
| Twitch Response | 0.23 | ++++ | ++++ |
*The combined presence of spot tenderness and palpable band will likely have high diagnostic value for sufficiently skilled examiners.
Recommended Criteria for Identifying a Latent or Active Trigger Point (Table 2.4B):
Essential Criteria:
- Taut band palpable (if muscle accessible).
- Exquisite spot tenderness of a nodule in a taut band.
- Patient's recognition of current pain complaint by pressure on the tender nodule (identifies an active trigger point).
- Painful limit to full stretch range of motion.
Confirmatory Observations:
- Visual or tactile identification of local twitch response.
- Imaging of a local twitch response induced by needle penetration of the tender nodule.
- Pain or altered sensation (in the distribution expected from a trigger point in that muscle) on compression of the tender nodule.
- EMG demonstration of spontaneous electrical activity characteristic of active loci in the tender nodule of a taut band.
The combination of spot tenderness in a palpable band and subject recognition of the pain are minimum acceptable criteria. There is no single examination that alone is a satisfactory criterion for routine clinical identification.
Differential Diagnosis and Confusions
Three possible sources of musculoskeletal pain are common and commonly overlooked: myofascial TrPs, fibromyalgia, and articular dysfunction that requires manual mobilisation. These three conditions often interact with one another, require different diagnostic examination techniques, and need significantly different treatment approaches.
| Initial Diagnosis | Some Likely TrP Sources | Manual Chapter (Vol. 1) |
|---|---|---|
| Angina Pectoris (atypical) | Pectoralis major | 42 |
| Appendicitis | Lower rectus abdominis | 49 |
| Atypical Angina | Pectoralis major | 42 |
| Atypical Facial Neuralgia | Masseter, Temporalis, Sternal division of SCM, Upper trapezius | 8, 9, 7, 6 |
| Atypical Migraine | Sternocleidomastoid, Temporalis, Posterior cervical | 7, 9, 16 |
| Back Pain, Middle | Upper rectus abdominis, Thoracic paraspinals | 49, 48 |
| Back Pain, Low | Lower rectus abdominis, Thoracolumbar paraspinals | 49, 48 |
| Dysmenorrhoea | Lower rectus abdominis | 49 |
| Earache (enigmatic) | Deep masseter | 8 |
| Epicondylitis | Wrist extensors, Supinator, Triceps brachii | 34, 36, 32 |
| Frozen Shoulder | Subscapularis | 26 |
| Occipital Headache | Posterior cervicals | 16 |
| Radiculopathy, C₆ | Pectoralis minor, Scalenes | 43, 20 |
| Scapulocostal Syndrome | Scalenes, Middle trapezius, Levator scapulae | 20, 6, 19 |
| Subacromial Bursitis | Middle deltoid | 28 |
| Temporomandibular Joint Disorder | Masseter, Lateral pterygoid | 8, 11 |
| Tennis Elbow | Finger extensors, Supinator | 35, 36 |
| Tension Headache | SCM, Masticatory muscles, Posterior cervicals, Suboccipital muscles, Upper trapezius | 7, 8–11, 16, 17, 6 |
| Thoracic Outlet Syndrome | Scalenes, Subscapularis, Pectoralis minor and major, Latissimus dorsi, Teres major | 20, 26, 43/42, 24, 25 |
| Tietze's Syndrome | Pectoralis major enthesopathy, Internal intercostals | 42, 45 |
Fibromyalgia Syndrome — Two of the three most common muscle pain syndromes, fibromyalgia and myofascial pain due to TrPs, are now recognised as quite separate clinical and etiological entities. Since both conditions are likely to cause severe muscle pain and frequently co-exist but need a different treatment approach, it is of great importance for the patient's sake that any clinician dealing with a patient who has muscle pain be able to clearly distinguish these two conditions.
| 1. History of widespread pain (left side, right side, above waist, below waist, axial skeleton). Present at least 3 months. |
| 2. Pain in at least 11 of 18 tender point sites on digital palpation at approximately 4 kg force. Sites include: bilateral suboccipital, low cervical (C5–C7 anterior intertransverse spaces), trapezius (midpoint upper border), supraspinatus (above scapular spine at origins), second rib (costochondral junctions), lateral epicondyle (2 cm distal), gluteal (upper outer quadrants), greater trochanter (posterior to prominence), knee (medial fat pad proximal to joint line). |
| Myofascial Pain (TrPs) | Fibromyalgia |
|---|---|
| 1 female : 1 male | 4–9 females : 1 male |
| Local or regional pain | Widespread, general pain |
| Focal tenderness | Widespread tenderness |
| Muscle feels tense (taut bands) | Muscle feels soft and doughy |
| Restricted range of motion | Hypermobile |
| Examine for trigger points | Examine for tender points |
| Immediate response to injection of TrPs | Delayed and poorer response to injection |
| 20% also have fibromyalgia | 72% also have active TrPs |
Articular Dysfunctions — Articular dysfunctions that require manual mobilisation make up one of the three major categories of musculoskeletal pain syndromes that are often overlooked. The pain in these syndromes is commonly caused by TrPs. The two conditions (TrPs and articular dysfunction) can aggravate each other: the increased tension of TrP taut bands and their facilitation of motor activity can maintain displacement stress on the joint, while abnormal sensory input from the dysfunctional joint can reflexly activate the TrP dysfunction.
Occupational Myalgias — Active TrPs are activated by acute overload or repeated overuse. A cardinal feature of myofascial TrPs is that they are activated either by acute overload or repeated overuse. Remarkably, among 56 occupational myalgia abstracts, NOT ONE indicated the authors had considered the possibility that myofascial TrPs may be contributing to the workers' problems.
'Trigger Points and Acupuncture — There is a high degree of correspondence (71% based on Melzack et al.s analysis) between published locations of TrPs and classical acupuncture points for the relief of pain. Classical acupuncture points are identified as prescribed points along meridians. However, central myofascial TrPs occur only in the midbelly region of a muscle belly; classical acupuncture points for pain are not found outside of the midbelly region. The mechanisms responsible for pain relief associated with acupuncture and TrP treatment have until very recently been enigmatic.
Nonmyofascial Trigger Points — Trigger points that refer pain also may be observed in what appears to be normal skin, in scar tissue, fascia, ligaments, and the periosteum. Scar TrPs (in skin or mucous membranes) refer burning, prickling, or lightning-like jabs of pain. Periosteal TrPs also refer pain in response to injection of hypertonic saline, just as the muscles do.
Posttraumatic Hyperirritability Syndrome — These patients may sometimes be identified as suffering from severe sudden-onset fibromyalgia that is associated with physical trauma and myofascial TrPs. This syndrome follows a major trauma such as an automobile accident, a fall, or a severe blow. The patient has constant pain that may be exacerbated by vibration of a moving vehicle, slamming of a door, loud noise, jarring, bumping, mild thumping, a pat on the back, a TrP injection, prolonged physical activity, and emotional stress (such as anger). Recovery from such stimulation is slow.
C. Muscle Structure and Function
Understanding the nature of myofascial TrPs requires understanding several aspects of basic muscle structure and function not usually emphasised.
Muscle Structure and Contractile Mechanism
A striated (skeletal) muscle is an assembly of fascicles, each of which is a bundle of roughly 100 muscle fibres. Each muscle fibre (a muscle cell) encloses approximately 1000–2000 myofibrils in most skeletal muscles. A myofibril consists of a chain of sarcomeres connected serially, end-to-end. The sarcomere is the basic contractile unit of skeletal muscle. Sarcomeres are connected to each other by their Z lines (or bands) like links in a chain.
Each sarcomere contains an array of filaments that consist of actin and myosin molecules which interact to produce contractile force. The myosin heads are a form of the enzyme adenosine triphosphatase (ATPase) that contacts and interacts with the actin to produce a contractile force.
- The middle panel of Figure 2.5 shows a resting-length sarcomere with complete overlap of actin and myosin filaments (maximum contractile force).
- During maximum shortening, the myosin molecules impinge against the "Z" band blocking further contraction.
- The lower panel shows a nearly fully stretched sarcomere with incomplete overlap of actin and myosin molecules (reduced contractile force).
Each sarcomere of a muscle can generate maximum force only in the midrange of its length but it can expend energy in the fully shortened position trying to shorten further. This principle is critical to understanding TrPs: a contraction knot keeps sarcomeres in a maximally shortened (energy-consuming) state.
Calcium is normally sequestered in the tubular network of the sarcoplasmic reticulum (SR) that surrounds each myofibril. Calcium is released from the SR when a propagated action potential reaches it from the surface of the cell through "T" tubules. Normally, after it has been released, the free calcium is quickly pumped back into the SR. The absence of free calcium terminates the contractile activity of the sarcomeres. In the absence of ATP, the myosin heads remain firmly attached ("failure to recock") and the muscle becomes stiff as in rigor mortis.
The Motor Unit
Motor units are the final common pathway through which the central nervous system controls voluntary muscular activity. A motor unit includes all of the muscle fibres innervated by one motoneuron. In summary, a motor unit includes one α-motoneuron and all of the muscle fibres that it supplies.
In postural and limb muscles, one motor unit supplies between 300 and 1500 muscle fibres. The smaller the number of fibres controlled by individual motoneurons (smaller motor units), the finer the motor control.
The Motor Endplate Zone
The motor endplate is the structure that links a terminal nerve fibre of the motoneuron to a muscle fibre. It contains the synapse where the electrical signal of the nerve fibre is converted to a chemical messenger (acetylcholine [ACh]) which in turn initiates another electrical signal in the cell membrane (sarcolemma) of the muscle fibre.
The endplate zone is the region where motor endplates innervate the fibres of the muscle. This region is now known as the motor point. The motor point is identified clinically as the area where a visible or palpable muscle twitch can be elicited in response to minimal surface electrical stimulation.
Location of Motor Endplates — Endplates in nearly all skeletal muscles are located near the middle of each fibre, midway between its attachments. Understanding the location of motor endplates is very important for the clinical diagnosis and management of myofascial TrPs. If, as appears to be the case, the pathophysiology of TrPs is intimately associated with endplates, one would expect to find TrPs only where there are motor endplates.
Neuromuscular Junction
The neuromuscular junction is a synapse which, like many in the CNS, depends on ACh as the neurotransmitter. The nerve terminal responds to the arrival of an action potential from the α-motoneuron by the opening of voltage-gated calcium channels. These channels allow ionised calcium to move from the synaptic cleft into the nerve terminal. The simultaneous release of many packets of ACh quickly overwhelms the barrier of cholinesterase in the synaptic cleft. Much of the ACh then crosses the synaptic cleft to reach the crests of the folds of the postjunctional membrane where the ACh receptors are located. The cholinesterase soon decomposes any remaining ACh, limiting its time of action.
The normal random release of individual packets of ACh from a nerve terminal produces well separated individual miniature endplate potentials (MEPPs). These individual MEPPs are not propagated and die out quickly.
Muscle Pain
Several endogenous substances are known to sensitise muscle nociceptors. These include bradykinin, E-type prostaglandins, and 5-hydroxytryptamine (serotonin), which in combination can potentiate sensitisation effects. The release of prostaglandins from nearby sympathetic fibres by noradrenalin may influence the TrP mechanism. There is evidence that prostaglandin-induced sensitisation of nociceptors is mediated by cyclic AMP. Other factors known to enhance sensitisation locally are increases in hydrogen ion concentration (pH decreased to 6.1) and substance P. Peripheral sensitisation of nociceptors would be responsible for local tenderness to pressure and most likely also for referred pain.
Several phenomena occurring at the spinal cord level can be related to referred pain. Injection of a pain-inducing substance into the muscular receptive field of a nociceptor neuron can result in the appearance of additional receptive fields in that limb — attributed to the "awakening" of "sleeping" nociceptive pathways in the spinal cord. An awareness of neuroplastic changes in the central nervous system is a relatively new and fundamental development with profound clinical implications. An acute nociceptive input can induce prolonged changes in the processing of nociceptive signals in the CNS that involve both functional and structural changes. More prolonged nociceptive input can induce more long-lasting changes that may not be reversible with time alone.
Much of the suffering from chronic pain is preventable if the acute pain is controlled promptly and effectively. Hong and Simons demonstrated that the length of treatment required for patients who had developed a pectoralis myofascial TrP syndrome as the result of whiplash injury was directly related to the length of time between the accident and the beginning of TrP therapy.
D. Nature of Trigger Points
Our current understanding of TrPs results from the convergence of two independent lines of investigation, one electrodiagnostic and the other histopathological. Fitting together the lessons from each leads to an Integrated Hypothesis that appears to explain the nature of TrPs.
Electrodiagnostic Characteristics of Trigger Points
The basis for the electrodiagnostic approach to the study of TrPs was anticipated by Weeks and Travell in 1957 when they reported that TrPs in the resting trapezius muscle exhibited a series of high-frequency spike-shaped discharges while at the same time adjacent sites in this muscle were electrically silent. In 1993, Hubbard and Berkoff reported similar electrical activity as being characteristic of myofascial TrPs.
When Simons, Hong, and Simons investigated the electrical activity in TrPs described by Hubbard and Berkoff, they employed a five-fold higher amplification and ten-fold increase in sweep speed. It was immediately apparent that there were two significant components:
- A consistently present, lower amplitude (maximum of about 60 μV) noise-like component.
- Intermittent and variable high-amplitude spike potentials.
The neutral term Spontaneous Electrical Activity (SEA) was adopted to identify these two components (or either one if only one is present at a given minute needle site). These three investigators used the same slow insertion technique reported by Hubbard and Berkoff.
The low-amplitude noise-like SEA component corresponds to what electromyographers recognise as normal motor endplate potentials (endplate noise). The high-amplitude spike component corresponds to endplate spikes. The similarity can be seen by comparing the recordings with endplate plate potentials illustrated in standard electrodiagnosis textbooks.
Spontaneous Electrical Activity (SEA) — The SEA here corresponds to an abnormal increase in the release of ACh packets by the motor nerve terminal. The resulting greatly increased number of MEPPs produces endplate noise and sustained partial depolarisation of the postjunctional membrane. This sustained depolarisation could cause a continuous release and uptake of calcium ions from the local sarcoplasmic reticulum, and produce sustained shortening (contracture) of sarcomeres.
Distribution of Active Loci — Active loci (where SEA occurs, or where SEA and spikes are found) were always found to be located within the endplate zone, the boundaries of which were determined independently. Active loci were four times more common in TrPs than in the endplate zone outside of a TrP (35:9). No active loci were observed in the taut band outside of the endplate zone. The SEA-type of endplate electrical activity is significantly related to myofascial TrPs.
Histopathological Characteristics of Trigger Points
Contraction knots are a characteristic histopathological finding in TrPs and in tender palpable nodules. They have been repeatedly noted, though their significance was not fully appreciated until the integrated hypothesis.
In 1976, Simons and Stolov used TrP criteria to examine canine muscles for a tender spot in a palpable taut band comparable to that observed in human patients. Some isolated, large, round muscle fibres and some groups of these darkly staining, enlarged, round muscle fibres appeared in cross sections. In longitudinal sections, the corresponding feature was a number of contraction knots. An individual knot appeared as a segment of muscle fibre with extremely contracted sarcomeres. This contracted segment showed a corresponding increase in diameter of the muscle fibre.
In 1996, Reitinger et al. biopsied in fresh cadavers the still-palpable nodules of myogelosis in the gluteus medius muscle. Cross sections showed the previously described, large, rounded, darkly staining muscle fibres and a statistically significant increase in the average diameter of muscle fibres in the myogelosis biopsies compared to non-myogelotic control biopsies from the same muscle. Electron microscopic cross sections showed an excess of A-Band and lack of the I-Band configuration — exclusive presence of A-Band in the absence of I-Band occurs only in fully contracted sarcomeres.
The structural features of contraction knots: each contraction knot is a segment of muscle fibre with extremely contracted sarcomeres. Normally, sarcomeres range in length from about 0.6 μm when fully shortened to about 1.3 μm when fully extended. Based on a minimum sarcomere length of 0.6 μm, the 100 sarcomeres of the contraction knot would extend 60 μm — within the 20 to 80 μm range of the length of normal motor endplates. Beyond the contraction knot, the muscle fibre becomes markedly thinned and consists of stretched sarcomeres to compensate for the contracted ones in the knot segment.
Integrated Trigger Point Hypothesis
The integrated hypothesis combines information from electrophysiological and histopathological sources. The energy crisis part of the hypothesis has been evolving for about 20 years and is compatible with recent electrodiagnostic findings, both of which fit the newly recognised histopathological picture.
Energy Crisis Component
This concept was developed to identify a pathophysiological process that could account for:
- The absence of motor unit action potentials in the palpable taut band of the TrP when the muscle was at rest.
- The fact that TrPs are often activated by muscle overload.
- The sensitisation of nociceptors in the TrP.
- The effectiveness of almost any therapeutic technique that restores the muscle's full stretch length.
The energy crisis concept was introduced in 1981 and was recently updated.
The energy crisis hypothesis postulates a vicious cycle of events (Figure 2.26):
- Initial Sustained Calcium Release from SR → Sustained Sarcomere Contracture → Increased Metabolism → Local Ischaemia → Energy Crisis → Failed Reuptake of Calcium into SR → (repeat)
The initiating event — such as trauma or a marked increase in the endplate release of ACh — can result in excessive release of calcium from the SR. This calcium produces maximal contracture of a segment of muscle which creates a maximal energy demand and chokes off local circulation. The ischaemia interrupts the energy supply, which causes failure of the calcium pump of the SR, completing the cycle.
The sustained contractile activity of the sarcomeres would markedly increase metabolic demands and would squeeze shut the rich network of capillaries that supply the nutritional and oxygen needs of that region. Circulation in a muscle fails during a sustained contraction that is more than 30% to 50% of maximum effort.
Integrated Trigger Point Hypothesis (Full)
The full integrated hypothesis (Figure 2.28 in the source) is based on continuous excessive ACh release from a dysfunctional motor nerve terminal into its synaptic cleft. Impaired cholinesterase function would potentiate the effect. The excessive ACh activates ACh receptors in the postjunctional membrane to produce greatly increased numbers of MEPPs. These potentials are so numerous that they superimpose to produce endplate noise and a sustained partial depolarisation of the postjunctional membrane.
Based on this hypothesis, the TrP region should have three demonstrable characteristics:
- Be higher in temperature than surrounding muscle tissue because of increased energy expenditure with impaired circulation to remove heat.
- Be a region of significant hypoxia because of ischaemia.
- Have shortened sarcomeres (contraction knots).
Evidence for local hypoxia in TrPs has been provided by oxygen probe studies in human patients with Myogelosen, documenting profound hypoxia in the central region of the induration (pO₂ falling abruptly to nearly zero as the probe approached the palpable border of the tender induration).
Confirmation of the integrated hypothesis requires identifying myofascial TrPs with tender nodules responsible for the patient's pain complaint; locating the SEA of an active locus electrodiagnostically; marking that location electrolytically with iron from the EMG needle; biopsying the site; fixing the biopsy by liquid nitrogen; and preparing longitudinal sections stained for iron, for acetylcholinesterase, and a base stain. If the iron-stained regions include contraction knots with motor endplates attached to them, this would greatly advance understanding of TrPs and the acceptance of their diagnoses.
Clinical Correlations of the Integrated Hypothesis
If multiple active loci are part of the same pathophysiological process as multiple contraction knots, and if this relationship applies equally to TrPs and to tender nodules, it would represent a major step forward in understanding enigmatic myogenic pain. Based on the integrated hypothesis:
- The taut band of a TrP is caused by the increased tension of involved muscle fibres both because of the tension produced by the maximally shortened sarcomeres in the contraction knot and because of the increased (elastic) tension produced by all the remaining elongated (and therefore thin) sarcomeres.
- The palpable nodule of TrP-related diagnoses (fibrositis, myogelosis) can be explained by the presence of multiple contraction knots — each sarcomere must maintain a nearly constant volume, so it becomes broader as it shortens.
- The spot tenderness of both TrPs and nodules would be the result of sensitised nociceptors sensitised by substances released as a result of the local energy crisis and tissue distress associated with endplate dysfunction.
- The enthesopathy (tenderness at the muscle attachment where the taut band terminates) is explained by the inability of the muscle attachment structures to withstand the unrelieved sustained tension produced by the taut band.
- The myoglobin response to massage of fibrositic nodules can be explained on the basis of the histopathological changes in nodules — repeated deep massage of the fibrositic nodules produced transient episodes of myoglobinuria not produced by similar massage of normal muscle.
Other Hypotheses
Pain-Spasm-Pain Cycle — The old concept of a pain-spasm-pain cycle does not stand up to experimental verification. Physiological studies show that muscle pain tends to inhibit, not facilitate, reflex contractile activity of the same muscle. In 1989, Ernest Johnson, editor of the American Journal of Physical Medicine, summarised overwhelming evidence that the common perception of muscle pain being closely related to muscle spasm is a myth.
Muscle Spindle Hypothesis — Hubbard and Berkoff initially suggested that the source of the EMG activity in TrPs was a dysfunctional muscle spindle. They gave three reasons for dismissing the possibility that these potentials might arise from motor endplates. However, existing literature and experimental findings contradict all three assertions: (1) the degree of localisation described under Active Loci and Spikes corresponds closely to that in the classical paper on the source of motor endplate potentials; (2) recent studies explicitly examined the distribution within the muscle and found activity chiefly in a TrP, to some extent also in the endplate zone, but not found outside of the endplate zone; and (3) muscle spindles are not concentrated just in the endplate zone where TrPs are found. Botulinum toxin A injection for TrP treatment acts only on the neuromuscular junction, effectively denerving that muscle cell — this supports the endplate hypothesis.
Neuropathic Hypothesis — Gunn proposed that the cause of TrP hypersensitivity is neuropathy of the nerve serving the affected muscle. There is much clinical evidence that compression of motor nerves can activate and perpetuate the primary TrP dysfunction at the motor endplate.
Fibrotic Scar Tissue Hypothesis — The concept that palpable firmness represents fibrotic (scar) tissue is based on the assumption that damaged muscle tissue has healed by scar formation. However, only two studies have reported biopsies of TrPs (one on dogs, one on humans); both presented strong evidence for the presence of contraction knots and neither found fibrosis. The rapid resolution of the palpable taut band with specific TrP treatment argues against the fibrosis explanation.
Local Twitch Response
The local twitch response (LTR) is a brisk transient contraction of the palpable taut band of muscle fibres elicited by mechanical stimulation of the TrP in that taut band. Mechanical stimulation may be produced by needle penetration of the TrP, by mechanical impact applied directly to the muscle (or applied through the skin over the TrP), or by snapping palpation of the TrP.
Clinically, the LTR is most valuable as a confirmatory sign when injecting a TrP — an LTR signals that the needle has reached a part of the TrP that will be therapeutically effective. It is often not practical to include the LTR as a primary diagnostic criterion of a TrP because when an LTR can be elicited, it is often prohibitively painful to the patient.
Topographic Extent of the Local Twitch Response — The pioneering study by Hong and Torigoe (1994) identified a trigger spot (comparable to the human TrP) in the rabbit biceps femoris muscle by locating a taut band using pincer palpation and testing along its length for a maximum twitch response to snapping palpation. The LTR was very sensitive to small displacements of only a few millimetres when the stimulus was applied to muscle fibres adjacent to the trigger spot, and was similarly attenuated by displacement a few centimetres along the same fibres that pass through the trigger spot. These findings correspond to the location of tenderness at TrPs in human patients.
LTR is a Spinal Reflex — The LTR is the motor response resulting from the activation of the involved motor unit(s) of the taut band. The LTR is propagated essentially as a spinal reflex that is not dependent on supraspinal influences. Evidence: transection of the spinal cord rostral to the segments supplying the biceps femoris caused the LTR to disappear due to spinal shock; as the animal recovered from spinal shock, the LTR slowly returned. However, after the motor nerve was severed, localised twitch responses became unobtainable and remained that way.
The α-motoneurons whose endplates suffer from excessive ACh release appear to be preferentially responsive to the strong sensory spinal input from the sensitised nociceptors. This possibility is reinforced by the observation that snapping palpation of one TrP resulted in simultaneous LTRs in the taut band of that TrP and in a taut band of another nearby muscle.
Summary: Key Concepts for Referencing in Muscle-Specific Chapters
The following concepts from Chapter 2 are referred to repeatedly throughout the muscle-specific chapters of the Manual:
- Taut Band
- A palpable rope-like induration in a muscle running the full length of the involved muscle fibres from attachment to attachment. It is caused by the sustained tension of involved muscle fibres at the contraction knot and by the elastic tension of the elongated sarcomeres on either side.
- Tender Nodule (Central Trigger Point, CTrP)
- The highly localised, exquisitely tender spot within the taut band at the location of the motor endplate zone. It is the palpable expression of multiple contraction knots.
- Attachment Trigger Point (ATrP)
- Localised tenderness at the musculotendinous attachment where the taut band terminates. Caused by the sustained tension exerted by the taut band at its attachment. Identified in the text by a red circle with a black border.
- Active Trigger Point
- A TrP that causes spontaneous pain at rest, or pain and/or referred pain with movement; that is tender to palpation with a referred pain pattern that is recognised by the patient as a familiar complaint; and that may produce referred motor and autonomic effects.
- Latent Trigger Point
- A TrP that is clinically quiescent with respect to spontaneous pain; is tender only when palpated; may have all the other clinical characteristics of an active TrP; and may restrict range of motion and cause weakness of the affected muscle.
- Key Trigger Point
- A TrP that activates a satellite TrP in its pain reference zone or in a muscle that it overloads. Inactivation of the key TrP often inactivates the satellite TrP without direct treatment.
- Satellite Trigger Point
- A TrP that is activated as a result of being in the pain reference zone or the zone of increased motor activity of a key TrP.
- Referred Pain Pattern
- The pattern of pain experienced at a distance from the responsible TrP. Characteristic of each muscle. The intensity and extent of the referred pain pattern depends on the degree of irritability of the TrP, not on the size of the muscle.
- Local Twitch Response (LTR)
- A brisk transient contraction of the taut band elicited by mechanical stimulation of the TrP. Propagated as a spinal reflex. Clinically the most specific sign of a TrP; most readily elicited by needle penetration.
- Spontaneous Electrical Activity (SEA)
- The characteristic electrical activity recorded at an active locus within a TrP consisting of low-amplitude continuous endplate noise and intermittent high-amplitude spikes. SEA corresponds to abnormal motor endplate activity. The SEA is always found within the endplate zone; never outside it.
- Contraction Knot
- A segment of a muscle fibre in which the sarcomeres are maximally contracted. The diameter of the fibre is markedly enlarged at the knot segment. The sarcomeres on either side of the knot are stretched thin to compensate. The contraction knot is the structural correlate of the active locus and the palpable nodule.
- Energy Crisis
- The vicious cycle maintaining a contraction knot: excessive ACh release → sustained sarcomere contracture → increased local metabolism → local ischaemia → failure of the calcium pump → further sustained calcium release → (repeat).
- Integrated Trigger Point Hypothesis
- The currently best-supported model of TrP pathophysiology, combining the energy crisis (metabolic/electrophysiological) component with the histopathological evidence of contraction knots. The TrP is essentially a region of many dysfunctional endplates, each associated with a section of muscle fibre that is maximally contracted (a contraction knot).
- Perpetuating Factors
- Factors that maintain TrP activity and interfere with healing. Often different from the factors that initially activated the TrP. Must be identified and corrected for effective lasting treatment. Covered in detail in Chapter 4 (not this chapter).
- Fibromyalgia vs. Myofascial TrPs
- Two distinct and separate conditions that frequently co-exist. Fibromyalgia: widespread pain, generalised tenderness, soft doughy muscles, hypermobile, female-predominant (4–9:1), characterised by central sensitisation. Myofascial TrPs: local or regional pain, focal tenderness, tense muscles (taut bands), restricted range of motion, equal sex ratio, characterised by focal peripheral endplate dysfunction.
See Also
- Chapter 3: Perpetuating Factors (when created)
- Chapter 4: Perpetuating Factors in Detail (when created)
- Travell & Simons Trigger Point Manual — Index
References
This page is based entirely on: Simons DG, Travell JG, Simons LS. Myofascial Pain and Dysfunction: The Trigger Point Manual. Volume 1: Upper Half of Body. 2nd ed. Baltimore: Williams & Wilkins; 1999. Chapter 2: General Overview, pp. 11–93.