Myofascial Pain in Athletes

Voluntary, or skeletal, muscle is the largest single organ of the human body and accounts for nearly 50% of the body’s weight. The number of muscles in the body depends on the degree of subdivision that is considered and on the number of variable muscles that are included. Not counting heads, bellies, and other divisions of muscles, the Nomina Anatomica reported by the International Anatomical Nomenclature Committee under the Berne Convention lists 200 paired muscles, or a total of 400 muscles. Any one of these muscles can develop myofascial trigger points (MTrPs). MTrPs are hyperirritable tender spots in palpable tense bands of skeletal muscle that refer pain and motor dysfunction, often to another location.

The myofascial pain syndromes (MPS) owe their ever-widening acceptance to the pioneering work of Travell and her later collaboration with Simons. In 1983, they combined their clinical experience in a detailed description of the multiple pain syndromes attributed to this disorder. In doing so, they further defined the major clinical components that are characteristic of myofascial pain, the most important being the TrP, the taut band, and the local twitch response.

Frequency

United States

MTrPs are extremely common and become a painful part of nearly everyone’s life at one time or another. Latent TrPs, which often cause motor dysfunction (eg, stiffness, restricted range of motion) without pain, are far more common than active TrPs that cause pain.

Active TrPs are commonly found 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 commonly involved.

Reports of the prevalence of MTrPs in specific patient populations are available. The data indicate a high prevalence of this condition among individuals with a regional pain complaint, as shown in Table 1.

Table 1. Prevalence of Myofascial Pain

Table

The wide range in the prevalences of myofascial pain caused by TrPs is likely due to differences in the patient populations examined and in the degree of chronicity, at least in part. Probably even more important are differences in the criteria used to diagnose MTrPs and, most important, differences in the training and skill of the examiners.

Functional Anatomy

Some isolated large round muscle fibers and some groups of these darkly staining, enlarged; round muscle fibers appear in cross-sections. In longitudinal sections, the corresponding feature is a number of contraction knots. An individual knot appears as a segment of muscle fiber with extremely contracted sarcomeres. This contractured segment has a corresponding increase in diameter of the muscle fiber.

The structural features of contraction knots presents a likely explanation for the palpable nodules and the taut bands associated with TrPs. Three single contraction knots can be seen scattered among normal muscle fibers. Beyond the thickened segment of the contracture muscle fiber at the contraction knot, the muscle fiber becomes markedly thinned and consists of stretched sarcomeres to compensate for the contracture ones in the knot segment. In addition, a pair of contraction knots separated by empty sarcolemma may represent one of the first irreversible complications that result from the continued presence of the contraction knot.

Sport Specific Biomechanics

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. In addition, 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 muscles (and likely other muscles, too), a degree of nerve compression that causes identifiable neuropathic electromyographic (EMG) changes is associated with an increase in the numbers of active TrPs. These TrPs may be activated by disturbed microtubular communication between the neuron and the endplate because the motor endplate is involved in the path physiologic process of the peripheral core TrP.

The histopathologic complications that could contribute to the chronicity of the condition and make treatment more difficult include the following:

• Distortion of the striations (sarcomere arrangement) in adjacent muscle fibers for some distance beyond the contraction knot (see Image 1). This produces unnatural shear forces between fibers that could seriously and chronically stress the sarcolemma of the adjacent muscle fibers. If the membrane were stressed to the point at which it became pervious to the relatively high concentration of calcium in the extracellular space, it could induce massive contracture that could compound the shear forces.
• The occasional finding of a segment of an empty sarcolemmal tube between 2 contractions knots may represent an additional irreversible complication of a contraction knot.

Latent TrPs can produce other effects characteristic of a TrP, including increased muscle tension and muscle shortening; but these do not produce spontaneous pain. Both active and latent TrPs can cause significant motor dysfunction. The same factors that are responsible for the development of an active TrP can, to a lesser extent, cause a latent TrP. An active key TrP in one muscle can induce an active satellite TrP in another. Inactivation of the key TrP often inactivates its satellite TrP without treatment of the satellite TrP itself.

The intensity and extent of the pattern of referred pain depends on the degree of irritability in the TrP, not on the size of the muscle. MTrPs in small, obscure, or variable muscles can be as troublesome to the patient as TrPs in large familiar muscles.

TrPs are activated directly by acute overload, overwork fatigue, direct impact trauma, and radiculopathy. TrPs can be activated indirectly by other existing TrPs, visceral disease, arthritic joints, joint dysfunctions, and emotional distress. Satellite TrPs are prone to develop in muscles that lie within the pain reference zone of key MTrPs or within the zone of pain referred from a diseased viscus, such as the pain due to myocardial infarction, gastric ulcer, cholelithiasis, or renal colic. A perpetuating factor increases the likelihood of overload stress that can convert a latent TrP to an active TrP.

With adequate rest and in the absence of perpetuating factors, an active TrP may spontaneously revert to a latent state. Pain symptoms disappear; however, occasional reactivation of the TrP by exceeding that muscle’s stress tolerance can account for a history of recurrent episodes of the same pain over a period of years.

Clinical

History

• Symptoms
  • Active TrPs produce a clinical complaint, usually pain, that the patient recognizes when the TrP is compressed digitally. The patient is aware of the pain caused by an active TrP, but he or she may or may not be aware of the dysfunction it causes.
  • Latent TrPs characteristically cause increased muscle tension and limit the stretch range of motion, which often escapes the patient’s attention or is simply accepted. The patient becomes aware of pain originating from a latent TrP only when pressure is applied to it. Spontaneous referred pain appears with increased irritability of the TrP; then, the TrP is identified as active.
  • The patient usually presents with complaints due to the most recently activated TrP. When this TrP is successfully eliminated, the pain pattern may shift to that of an earlier key TrP that must also be inactivated. If the key TrP is inactivated first, the patient may recover without further treatment.
  • Patients with active MTrPs usually complain of poorly localized, regional, aching pain in subcutaneous tissues, including muscles and joints. They rarely complain of sharp, clearly localized coetaneous-type pain. The myofascial pain is often referred away from the TrP in a pattern that is characteristic for each muscle. Sometimes, the patient is aware of numbness or paresthesia rather than pain.
• Dysfunction
  • In addition to the clinical symptoms produced by the sensory disturbances of referred pain, dysesthesias, and hypoesthesia’s, patients can also have clinically important disturbances of autonomic and motor functions.
  • Disturbances of autonomic functions
    • Disturbances of autonomic functions caused by TrPs include abnormal sweating, persistent lacrimation, persistent coryza, excessive salivation, and pilomotor activities.
    • Related proprioceptive disturbances caused by TrPs include imbalance, dizziness, tinnitus, and distorted perception of the weight of lifted objects.
  • Disturbances of motor functions
    • Disturbances of motor functions caused by TrPs include spasm of other muscles, weakness of the involved muscle function, and 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, with further weakening and deconditioning of the involved muscle.
    • The combination of weakness in the hands and loss of forearm muscle coordination makes the grasp unreliable. Objects sometimes slip unexpectedly from the patient’s grasp. The weakness results from reflex motor inhibition and characteristically occurs without atrophy of the affected muscle. Patients are prone to intuitively substitute muscles without realizing that, for instance, they are carrying the grocery bag in the nondominant but now stronger arm.
  • The motor effects of TrPs on the muscle in which they are located are considered in detail under Surface electromyography in Other Tests.
• Sleep disturbances
  • Disturbance of sleep can be a problem for patients with a painful TrP syndrome. Authors of a series of studies have shown that many sensory disturbances, including pain, can seriously disturb the patient’s sleep.
  • This sleep disturbance can, in turn, increase pain sensitivity the next day. Active MTrPs become more painful when the muscle is held in the shortened position for long periods and if body weight compresses the TrP. Thus, for patients with active TrPs, sleep positioning can be critical to prevent unnecessary disturbances of their sleep.

Physical

Each muscle has a characteristic elicited referred pain pattern that, for active MTrPs, is familiar to the patient. Without a laboratory test or imaging method, diagnosis of MTrPs depends entirely on history and physical examination. MTrP symptoms follow muscle overload, are activated acutely by sudden overload, or develop gradually with prolonged contractions or repetitive activity. The diagnostic skill required depends on considerable innate palpation ability, authoritative training, and extensive clinical experience.

Pain prevents a muscle with a MTrP from reaching its full stretch range of motion and also restricts its strength and/or endurance. Clinically, the lip is a localized spot of tenderness in a nodule within a palpable taut band of muscle fibers. Restricted stretch range of motion and a palpable increase in muscle tenseness (ie, decreased compliance) are more severe in more active MTrPs.

Active MTrPs are identified when patients recognize the pain induced by applying pressure to a MTrP. The taut band fibers usually respond with an MTrP when the taut band is accessible and when the TrP is stimulated by properly applied snapping palpation. The taut band fibers have a consistent twitch response when a needle penetrates the MTrP.

• Taut band
  • By gently rubbing across the direction of the muscle fibers in a superficial muscle, the examiner can feel a nodule at the MTrP and ropelike indurations that extends from this nodule to the attachment of the taut muscle fibers 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, sometimes immediately. See Image 2.
• Tender nodule
  • Palpation along the taut band reveals a nodule exhibiting a highly localized and exquisitely tender spot that is characteristic of an MTrP. When the spot is tested for tenderness, displacement of the algometer by 2 cm produces a statistically significant decrement in pain threshold algometer readings. Clinically, displacement of the application of pressure by 1-2 mm at an MTrP can result in a markedly reduced pain response.
  • This strong localization of tenderness in the vicinity of an MTrP corresponds to the localized sensitivity of the experimental muscle for eliciting TrPs as demonstrated in rabbit experiments. A 5-mm displacement to either side of the trigger spot (at right angles to the taut band) results in almost total loss of response. However, the response fades out more slowly when stimulated over a range of several centimeters from the trigger spot along the taut band.
• Recognition: Application of digital pressure on either an active or latent MTrP can elicit a referred pain pattern characteristic of that muscle. However, if the patient recognizes the elicited sensation as a familiar experience, this establishes the MTrP as being active and is one of the most important diagnostic criteria available when the palpable findings also are present. Similar recognition is observed frequently when a needle penetrates the MTrP and encounters an active locus.
• Referred sensory signs: In addition to referring pain to the reference zone, MTrPs may refer other sensory changes such as tenderness and dysesthesias.
• Local twitch response: Snapping palpation of the TrP frequently evokes a transient twitch response of the taut band fibers. Twitch responses can be elicited both from active and latent TrPs. Hubbard at al showed that no difference was noted in twitch responses whether elicited by snapping palpation or by needle penetration. See Image 3.
• Limited range of motion
  • Muscles with active MTrPs 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 fibers are already under substantially increased tension at rest length.
  • The limitation of stretch due to pain is not as great with active movement as with passive lengthening of the muscle; this finding at least partly due to reciprocal inhibition. When the TrP is inactivated and the taut band is released, range of motion returns to normal.
  • The degree of limitation produced by MTrPs is much more marked in some muscles (eg, subscapularis) than in other muscles (eg, latissimus dorsi).
• 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 the patient attempts to contract the muscle when it is in a shortened position.
• Weakness
  • Although weakness is generally characteristic of a muscle with active myofascial MTrPs, the magnitude is varied from muscle to muscle and from subject to subject.
  • EMG studies indicate that, in muscles with active MTrPs, the muscle starts out fatigued, it fatigues more rapidly, and it becomes exhausted sooner than normal muscles. The weakness may reflect reflex inhibition of the muscle by the MTrPs.

Causes

Causes of myofascial pain include or are related to the following:

• The lack of motor unit action potentials due to the endogenous contracture of the contractile elements, rather than a nerve-initiated contraction of the muscle fibers
• The frequency with which muscle overload activates TrPs, which may reflect the marked mechanical vulnerability of the synaptic cleft region of an endplate
• The release of substances that could sensitize nociceptors in the region of the dysfunctional endplate of the TrP as a result of tissue distress caused by the energy crisis
• The effectiveness of essentially any technique that elongates the TrP portion of the muscle to its full stretch length even briefly, which could break the cycle that includes energy-consuming contractile activity
• Laborers who exercise their muscles heavily every day are less likely to develop active TrPs than sedentary workers who are prone to intermittent episodes of vigorous physical activity. This author’s clinical experience supports this observation.

Author: Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver