Myofascial Pain in Athletes

The myofascial pain syndromes (MPS) owe their ever-widening acceptance to the pioneering work of Travell and her later collaboration with Simons.[3, 4] 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. See the image below.

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.

United States data

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 (Open Table in a new window)

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.

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 contractured muscle fiber at the contraction knot, the muscle fiber becomes markedly thinned and consists of stretched sarcomeres to compensate for the contractured 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.

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 pathophysiologic 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 the image below). 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.

  Myofascial pain in athletes. Schematic of a trigger point complex of a muscle in longitudinal section.A: The central trigger point (CTrP) in the endplate zone contains numerous electrically active loci and numerous contraction knots. A taut band of muscle fibers extends from the trigger point to the attachment at each end of the involved fibers. The sustained tension that the taut band exerts on the attachment tissues can induce a localized enthesopathy that is identified as an attachment trigger point (ATrP).B: Enlarged view of part of the CTrP shows the distribution of 5 contraction knots. The vertical lines in each muscle fiber identify the relative spacing of its striations. The space between 2 striations corresponds to the length of one sarcomere. The sarcomeres within one of these enlarged segments (ie, contraction knot) of a muscle fiber are markedly shorter and wider than the sarcomeres in the neighboring normal muscle fibers, which are free of contraction knots.

• 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.

Complications

The single muscle MPSs usually are acute and follow an episode of muscle overload. In some cases, the pain persists and spreads to other, usually synergistic, muscles. This is referred to as a chronic regional myofascial syndrome.

Many perpetuating factors encourage transformation to a more widespread muscle pain problem. Mechanical factors include postural stress, muscle imbalances, and skeletal asymmetries. These can put additional stress on surrounding muscles, leading to spread of dysfunction and pain. Systemic perpetuating factors purportedly include anything jeopardizing the energy supply to muscle (ie, anemia, endocrine imbalances, low thyroid function, vitamin deficiencies). Advise patients to avoid these mechanical and systemic factors if possible.

Chronic regional myofascial syndromes are conceptually close to the malignant, metastasizing fibromyalgia referred to by Bennett.

Return to play

Athletes should avoid strenuous activity during sports, and they should always use stretching techniques prior to competitions or practice.

 

The ultimate goal is to educate patients and (1) to provide them with the means to manage their own muscle pain disorder, (2) to eliminate their dependence on healthcare providers, (3) to eliminate contributing factors, providing prolonged stretch of the affected muscle, and aerobic exercises.[5]

On performing a task, the patient must learn to keep the muscles mobilized, and not held fixed in a contracted position. Muscle fibers need to alternately contract and relax to provide blood flow and replenish their energy supply.

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 cutaneous-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 hypesthesias, 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, 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.

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.[6, 5]  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 a 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 a ropelike induration 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 the image below.

    Myofascial pain in athletes. Cross-sectional drawing shows flat palpation of a taut band and its trigger point.Left: Skin pushed to one side to begin palpation (A). The fingertip slides across muscle fibers to feel the cord-line texture of the taut band rolling beneath it (B). The skin is pushed to other side at completion of movement. This same movement performed vigorously is snapping palpation (C).Right: Muscle fibers surrounded by the thumb and fingers in a pincer grip (A). The hardness of the taut band is felt clearly as it is rolled between the digits (B). The palpable edge of the taut band is sharply defined as it escapes from between the fingertips, often with a local twitch response (C).

• Tender nodule

  • Palpation along the taut band reveals a nodule exhibiting a highly localized and exquisitely tender spot that is characteristic of a 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 a MTrP can result in a markedly reduced pain response.

  • This strong localization of tenderness in the vicinity of a 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 the image below.

  Myofascial pain in athletes. Longitudinal schematic drawing of taut bands, myofascial trigger points, and a local twitch response. A: Palpation of a taut band (straight lines) among normally slack, relaxed muscle fibers (wavy lines). B: Rolling the band quickly under the fingertip (snapping palpation) at the trigger point often produces a local twitch response that usually is seen most clearly as skin movement between the trigger point and the attachment of the muscle fibers.

• 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.

No laboratory test or imaging technique is generally established as useful in the diagnosis of TrPs.[5, 6]

Three measurable phenomena help to objectively substantiate the presence of characteristic TrP phenomena, and all three are valuable as research tools. Two of them, surface electromyography (EMG) and ultrasonography, also have much potential for clinical application in the diagnosis and treatment of TrPs.[5, 6]  For example, in a randomized, controlled trial that included 33 patients with upper trapezius myofascial pain, low-intensity continuous ultrasound treatment produced a significant reduction in pain scores.[7]

In addition to EMG recording, ultrasonography provides a second way of substantiating and studying the LTR and it also has a strong potential for providing a much needed available imaging technique that could be widely used to objectively substantiate the clinical diagnosis of TrPs.[6, 5, 8]

This test would require the examiner to use the skill-demanding snapping palpation technique, or to insert a needle into the TrP, to elicit the twitch response.[9]

Surface electromyography

TrPs cause distortion or disruption of normal muscle function.

Functionally, the muscle with the TrP evidences a 3-fold problem: It exhibits increased responsiveness, delayed relaxation, and increased fatigability. Together, these effects increase muscle overload and reduce its work tolerance. In addition, the TrP can produce referred spasm and referred inhibition in other muscles.

With the recent appearance of online computer analysis of EMG amplitude and mean power spectral frequency, a few pioneer investigators have reported the effects of TrPs on muscle activity. The reports indicate that TrPs can influence the motor function of the muscle in which they occur and that their influence can be transmitted through the central nervous system to other muscles.

To date, the number of well-controlled studies to establish the clinical reliability and application of these observations is insufficient, but findings from the few reports of these TrP effects are promising.

The strong clinical effects of TrPs on sensation, as evidenced by TrP tenderness and referred pain, are well documented.

Strong cutaneous stimuli (eg, electric shocks) are well known to cause reflex motor effects (eg, flexion reflex). If the skin can modulate motor activity and if TrPs can modulate sensory activity, the fact that TrPs can also strongly affect motor activity should not be surprising. In fact, the motor effects of lips may be the most important influence they exert, because the motor dysfunction they produce may result in overload of other muscles and spread the TrP problem from muscle to muscle.

Accumulating evidence now indicates that the muscles targeted for referred spasm from TrPs also usually have TrPs themselves. These motor phenomena of TrPs deserve serious competent research investigation.

An increased responsiveness of some affected muscles is indicated by abnormally high amplitude of EMG activity when the muscle is voluntarily contracted and loaded.[10] Clinical evidence suggests that some muscles tend to be shortened and abnormally excitable, while others appear to be weak and inhibited.

Fatigability noted at EMG and in terms of work tolerance, of the trapezius muscle that had MTrPs is accelerated compared to a contralateral muscle that was pain-free. The EMG amplitude increased and median power frequency decreased significantly in the involved muscle compared to the uninvolved muscle. Both of these changes are characteristic of initial fatigue.

Median power frequency generally is accepted as a valid criterion of muscle fatigue. Delayed recovery following fatiguing exercise commonly is seen in patients with muscle-related cumulative trauma disorder (CTD). MTrPs were very common in the involved muscles in this group.

Delayed relaxation is commonly seen in muscle-overload work situations. This failure to relax is a common surface EMG finding during repetitive exercises of muscles with MTrPs.

In addition, the TrP can induce motor activity (eg, referred spasm) in other muscles.

Algometry

Sensitivity to pain in patients with TrPs can be measured as the pain threshold to electrical stimulation or applied pressure. The use of pressure algometry is most commonly reported.

Pressure algometry involves the induction of a specific pain level in response to a measured force perpendicularly applied to the skin. The following 3 endpoints are reported: (1) onset of local pain (ie, pressure pain threshold), (2) onset of referred pain (ie, referred pain threshold), and (3) intolerable pressure (ie, pain tolerance).

Most commonly, the pressure required to reach pain threshold is directly measured on a spring scale that is calibrated in kilograms, newtons, or rounds. Because the pressure is applied through a circular footplate, its diameter is a factor, and the actual measurement is stress (in kilograms per square centimeter) applied to skin.

For example, one of the most common algometers has a footplate area of 1 cm2; therefore, its meter, which provides readings in kilograms, is numerically the same as the number of kilograms per square centimeter, and no numeric conversion is needed.

Thermography

Thermograms can be recorded by using infrared radiometry or films of liquid crystal. Recording infrared radiation (ie, electronic thermography) with computer analysis provides a powerful tool for tile accurate rapid visualization of skin temperature changes over large areas of the body. This technique can demonstrate cutaneous reflex phenomena characteristic of MTrPs. The less expensive contact sheets of liquid crystal have limitations that make reliable interpretation of the findings considerably more difficult.

Each of these thermographic techniques is used to measure the skin surface temperature to a depth of only a few millimeters. The temperature changes correspond to changes in the circulation within, but not beneath, the skin. The endogenous cause of these temperature changes is usually sympathetic nervous system activity. Therefore, thermographic changes in skin temperature are comparable in meaning to changes in skin resistance or changes in sweat production. However, electronic infrared thermography is superior to these other two measures (ie, infrared radiometry or with films of liquid crystal) in convenience and in spatial as well as temporal resolution.

In summary, Fisher's research studies indicate that the finding a hot spot on the thermogram is not sufficient to identify a TrP beneath it. A similar temperature change can be expected in radiculopathy, articular dysfunction, enthesopathy, or local subcutaneous inflammation. The thermographic hot spot of a TrP is described as a discoid region 5 to 1 (3 cm in diameter, displaced slightly from directly over the TrP).

Procedures to confirm diagnosis of MPS

The first international symposium on myofascial pain and fibromyalgia was held in 1989. It marked one of the first meetings of the principal proponents of the 2 major muscle pain syndromes. In the proceedings of that symposium, Simons listed the clinical criteria for diagnosis of MPS.[6, 5]

• Clinical criteria for the diagnosis of MPS caused by active TrPs

  • To make the clinical diagnosis of MPS, the findings should include 5 major criteria and at least 1 of 3 minor criteria. The 5 major criteria include the following:[6, 5]

    • Regional pain complaint

    • Pain complaint or altered sensation in the expected distribution of referred pain from a MTrP

    • Taut band palpable in an accessible muscle

    • Exquisite spot tenderness at 1 point along the length of the taut band

    • Some degree of restricted range of motion, when measurable

  • The 3 minor criteria include the following:

    • Reproduction of clinical pain complaint, or altered sensation, by pressure on the tender spot

    • Elicitations of a local twitch response by transverse snapping palpation at the tender spot or by needle insertion into the tender spot in the taut band

    • Pain alleviated by elongating (stretching) the muscle or by injecting the tender spot (TrP)

  • Additional symptoms, such as weather sensitivity, sleep disturbance, and depression, often are present, but they are not diagnostic because they may be attributable to chronic, severe pain perpetuated by multiple mechanical and/or systemic perpetuating factors.

• The required features include regional pain, referred pain, or disturbed sensation in a predicted location; a taut band; a tender point along the taut band; and restricted range of motion.

• One of 3 of the following minor criteria also must be present:

  • Pain complaint reproduced by pressure on the tender spot

  • A local twitch response

  • Relief of the pain by stretching or injecting

• At the same time, Simons listed research criteria for the identification of TrPs. To qualify, the point must be exquisitely tender, located in a taut band of a muscle with restricted range of motion, refer pain when pressed or needled, and exhibit a twitch response when needled.

Rehabilitation program

Physical therapy

Effective treatment of an MPS caused by TrPs usually involves more than simply applying a procedure to TrPs.[5, 11, 12] Often, it is necessary to consider and deal with the cause that activated the TrPs, to identify and correct any perpetuating factors (which often are different than what activated the TrPs), and to help the patient restore and maintain normal muscle function. Common misconceptions about the treatment of TrPs include the following:

• Simply treating the TrP should be sufficient, especially if the stress that activated the TrP is not recurrent and if no perpetuating factors are present.

  • In this case, the TrP is likely to be reactivated by the same stress.

  • Ignoring perpetuating factors invites recurrence. After the TrPs have persisted for some time, failure to retrain the muscle to normal function or failure to reestablish its full-stretch range of motion results in a degree of persistent motor dysfunction.

• The pain cannot be as severe as the patient says and must be largely psychogenic.

  • The patients are trying to communicate their degree of pain. Believe them. The pain feels severe to them. Patients in a general medical practice rated their pain as severe as or more severe than pain from other causes such as pharyngitis, cystitis, angina, and herpes zoster.

  • An appreciable amount of the pain reported by many patients with fibromyalgia comes from their TrPs. The pain of fibromyalgia rates fully as severe as the pain of rheumatoid arthritis. It is severe enough to cause central nervous system changes characteristic of chronic pain.

  • Because of their chronic lip and fibromyalgia pain, these patients often develop pain behaviors that tend to reinforce dysfunction and further pain. Many patients experience grievous and needless degree and duration of pain, because a series of clinicians unacquainted with MTrPs erroneously (covertly if not overtly) diagnosed a psychogenic condition.

• MPSs 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 1 or 2 weeks, if the muscle is not overstressed (used within tolerance, which may be limited) and if no perpetuating factors are present. Otherwise, if the acute syndrome is not properly managed, it evolves needlessly into a chronic MPS.

• Relief of pain by treatment of skeletal muscles for MTrPs rules out serious visceral disease.

  • Because of the referred pain nature of visceral pain, application of vapocoolant spray or infiltration of a local anesthetic into the somatic reference zone can temporarily relieve the pain of myocardial infarction, angina, and acute abdominal disease with no effect on the visceral pathology.

Rehabilitation program: The treatment approaches include the use of simple muscle stretch, augmented muscle stretch, post-isometric relaxation, reciprocal inhibition, slow exhalation, eye movement, TrP pressure release, massage, range of motion, heat, ultrasound, high-voltage galvanic stimulation, drug treatment, biofeedback, and new injection techniques.[6]

Physical therapy includes simple muscle stretch, augmented muscle stretch, post-isometric relaxation, reciprocal inhibition, slow exhalation, eye movement, TrP pressure release, massage, range of motion, heat, ultrasound, and high-voltage galvanic stimulation.[6, 13, 14]

A study by Yeste-Fabregat et al showed that Tecar therapy (diathermy) can raise local temperature in the medial gastrocnemius and decrease local pain at the TrP in professional male basketball players with latent MTrPs.[15]

A meta-analysis by Zhou et al demonstrated that the addition of exercise rehabilitation to a single-intervention clinical treatment for MPS significantly reduced pain and improved functioning in patients with MTrPs.[16]

Medical issues/complications

Table 2. Myofascial Trigger Points Mistakenly Diagnosed as Other Conditions (Open Table in a new window)

Table 3. Differences in Clinical Features that Distinguish Myofascial Pain due to TrPs from Fibromyalgia (Open Table in a new window)

Complications of injections

Pneumothorax by aiming the needle at an intercostal space: The only exception is when the intercostal muscles must be injected. This should be performed with great care.

The location of the needle tip can be misjudged readily when using a long slender needle. Furthermore, the needle should be inserted straight, avoiding any side pressure that might bend it, deflecting the tip an unknown distance to one side.

It is especially important to avoid using a needle with a burr at the tip because it causes unnecessary bleeding. When the tip of a disposable needle contacts bone, the impact frequently curls the tip to produce a fishhook burr that feels scratchy and drags as the needle is drawn through tissues.

Contraindications

Contraindications to TrP injections are as follows:

• Patients on anticoagulation therapy

• If the patient has taken aspirin within 3 days of injection

• Tobacco smokers, unless they have stopped smoking and have taken at least 500 mg of timed-release vitamin C for 3 days prior to injection

• Patients who have an inordinate fear of needles

• Patients should avoid strenuous activity and sports for 10 days.

Consultations

The clinical importance of MTrPs to practitioners has been described in the literature for acupuncturists, anesthesiologists, chronic pain managers, dentists, family practitioners, gynecologists, neurologists, nurses, orthopedic surgeons, pediatricians, physical therapists, physiatrists, rheumatologists, and veterinarians.

Other treatments and techniques

Botulinum A toxin injection

The clinical effectiveness of botulinum A toxin injection for the treatment of MTrPs helps to substantiate dysfunctional endplates as an essential part of the pathophysiology of TrPs (see the images below).[17, 18, 19, 20, 21, 22] This toxin specifically acts only on the neuromuscular junction, effectively denervating that muscle cell.[23]

Stretch and spray

Infants have been observed with point tenderness of the rectus abdominis muscle and colic, both of which were relieved by sweeping a stream of vapocoolant spray over the muscle, which helps to inactivate MTrPs.

The sequence of steps when stretching and spraying any muscle for MTrPs is shown in the image below.[24]

The sequence of steps to use when stretching and spraying any muscle is as follows:

• The patient is supported in a comfortable relaxed position.

• One end of the muscle is anchored.

• Skin is sprayed with repeated parallel sweeps of the Vapo coolant over the length of the muscle in the direction of pain pattern.

• After the first sweep of spray, pressure is applied to take up the slack in the muscle and is continued as additional sweeps of spray are applied.

• Sweeps of the spray are extended to cover the referred pain pattern.

• Steps 3, 4, and 5 may be repeated 2 or 3 times until the skin becomes cold to the touch or when the range of motion reaches maximum.

Technique of spray and stretch

• For example, treatment for right levator scapulae TrPs; the direction and pattern of the Vapo coolant spray follows the muscle fibers (see the image below).

  Myofascial pain in athletes. Schematic drawing showing how the jet stream of Vapo coolant is applied.

• During the distraction of the spray, the operator presses the patient's head forward and to the opposite side, while using the elbow to press the patient's shoulder down and back. Similar techniques are applied to most other TrPs. The key ingredient is the prolonged stretch of the affected muscle.

• Unidirectional sweeps cover, first, parallel lines of skin over those muscle fibers that are stretched the tightest, then over the rest of the muscle and its pain pattern. Sequential sweeps of spray should follow the direction of the muscle fibers and progress toward the referred pain zone.

TrP injection technique

• To prevent bleeding, the fingers of the palpating hand should be spread apart, maintaining tension on the skin to reduce the likelihood of subcutaneous bleeding where the needle has penetrated (see the image below). Also, during the injection, the fingers exert pressure around the needle tip to provide homeostasis in deeper tissues. When the angle of the needle is changed, the direction of pressure changes.

  Myofascial pain in athletes. Schematic top view of 2 approaches to the flat injection of a trigger point area in a palpable taut band. Injection away from the fingers (A) and injection toward the fingers (B).

• The physician should avoid inserting the needle to the hub where the needle is most likely to break off. Some additional depth of penetration can be obtained safely by indenting the skin and subcutaneous tissues with a finger beside the needle as illustrated in the image below.

  Myofascial pain in athletes. C. Z. Hong's technique. Finger pressure beside the needle is used to indent the skin, subcutaneous, and fat tissues so that the needle can reach the trigger point in a muscle that would be inaccessible otherwise.

• The importance of distinguishing between central TrPs, ie, in the central portion of the muscle belly and attachment TrPs when injecting, is illustrated in the image below.

  Myofascial pain in athletes. Diagrammatic representation of pre-injection sites (open circles) and injection sites (solid circles) of local anesthetic to the trigger point. The enclosed stippled area represents the taut band. This diagram distinguishes the central trigger point within the large broken circle from the attachment trigger points located at the myotendinous junction and at the attachment of the tendon to the bone. Each of these 3 trigger point regions can be identified by their individual spot tenderness and anatomical locations. No rationale is apparent for injecting the part of the taut band that lies between the central trigger point and the attachment trigger point (solid circles numbers 7-10).

• The increased capillary fragility characteristic of a low serum vitamin C level can cause excessive bleeding in muscles injected for TrPs. Capillary hemorrhage augments postinjection soreness and leads to unsightly ecchymoses. A frequent source of increased bleeding due to low vitamin C is tobacco. Mega-dose vitamin C therapy daily for 1 week should correct this deficiency. At least 500 mg of timed-release vitamin C 3 times daily is recommended for a minimum of 3 days prior to injection of TrPs. A daily dose of aspirin increases the susceptibility to bleeding. The patient should take no aspirin for 3 days before TrP injection or needling.[25]

Eftekharsadat et al found corticosteroid TrP injection provided greater short-term control of pain and disability than extracorporeal shock wave therapy (ESWT) did in patients with MPS of the quadratus lumborum muscle. However, after 4 weeks, ESWT was more effective than corticosteroid TrP injection in improving quality of life and reducing disability.[26]

Benito-de-Pedro et al compared a single session of deep dry needling with ischemic compression in a latent MTrP of the shortened triceps surae in 34 triathletes. The researchers assessed ankle dorsiflexion range of motion and dynamic and static plantar pressures before and after treatment and found no statistically significant differences between the two treatment groups.[27]

Anti-inflammatory agents, including corticosteroids and analgesics, are generally not useful, and their administration should be avoided. Localized and regional muscle pain syndromes often respond to specific localized therapies. The most common treatment for localized muscle pain is injection. Take great care in locating the TrP, watch for the twitch response on the muscle, and then enter the muscle with the needle.[28]

Class Summary

Amide derivative local anesthetic used to minimize postinjection soreness.

Lidocaine HCL (Xylocaine)

Has rapid onset of action. Stabilizes neuronal membrane by inhibiting the sodium flux required for the initiation and conduction of impulses. In addition, causes inhibition of release of neurotransmitters (eg, substance P), ATP from nociceptive afferent C fibers, modulation in information transfer along primary afferents, and central sympathetic blockade with decrease in pain-induced reflex vasoconstriction.

Procaine (Novocaine)

Regional anesthesia for treatment of painful conditions (eg, neuropathic pain, reflex sympathetic dystrophy, myofascial pain). Least myotonic and has lowest systemic toxicity among commonly used local anesthetics. Procaine is the ester of p-aminobenzoic acid and ethanol with a tertiary diethylamino group attached at the other end of the alcohol. Stabilizes neuronal membrane and prevents the initiation and transmission of impulses. Has a rapid onset of action and relatively short duration depending on anesthetic technique, type of block, concentration, and patient. Greater solution concentration does not increase anesthetic effect.

Class Summary

Botulinum toxin type A (BTA) binds irreversibly to presynaptic cholinergic nerve terminals, which includes the terminals of motor nerve supplying skeletal muscle-fiber endplates. Since the primary dysfunction of motor endplates associated with the TrP phenomenon appears to be excessive release of acetylcholine (ACh), injections into the TrP of a substance (eg, BTA) that only blocks ACh should be specific TrP therapy. This toxin specifically acts only on the neuromuscular junction, effectively denervating that muscle cell.

OnabotulinumtoxinA (BOTOX®)

BTA blocks neuromuscular transmission through a 3-step process, as follows: (1) blockade of neuromuscular transmission; BTA binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. (2) BTA is internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. (3) BTA blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. The toxin does not affect the synthesis or storage of acetylcholine or the conduction of electrical signals along the nerve fiber.

Typically, a 24-72 h delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 mo.

This purified neurotoxin complex is a vacuum-dried form of purified BTA, which contains 5 ng of neurotoxin complex protein per 100 U.

BTA has to be reconstituted with 2 mL of 0.9% sodium chloride diluent. With this solution each 0.1 mL results in 5 U dose. Patient should receive 5-10 injections per visit.