Myofascial Pain in Athletes

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Background: Voluntary, or skeletal, muscle is the largest singleorgan of the human body and accounts for nearly 50% of the

bodys weight. The number of muscles in the body depends on thedegree of subdivision that is considered and on the number ofvariable muscles that are included. Not counting heads, bellies, and

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Myofascial Pain in Athletes

Last Updated: December 4, 2002

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Synonyms and related keywords: myofascial pain syndromes, trigger points,

MPS, myofascial trigger points, TrPs

AUTHOR INFORMATION Section 1 of 11

Author InformationIntroductionClinicalDifferentialsWorkupTreatmentMedicationFollow-upMiscellaneousPicturesBibliography

Author: Auri A Bruno, MD, MS, Associated Physiatrist, ClinicalAssistant, Discipline of Physical Medicine and Rehabilitation, SaoPaulo Federal University, Brazil

Auri A Bruno, MD, MS, is a member of the following medical

societies: American Academy of Physical Medicine andRehabilitation, International Rehabilitation Medicine Association,and International Society of Physical and Rehabilitation Medicine

Editor(s): Anthony J Saglimbeni, MD, Education Director, ClinicalAssistant Professor, Departments of Family, Internal and SportsMedicine, and Pediatrics, University of California at San Diego;Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor,Pharmacy, eMedicine; Russell White, MD, Clinical AssociateProfessor, Department of Family Medicine, University of SouthFlorida College of Medicine; Director, Center for Sports Medicine,Associate Program Director, Bayfront Medical Center; Jon

Whitehurst, MD, Fellow, Sports Medicine, Southern CaliforniaOrthopedic Institute; and Sherwin SW Ho, MD, AssociateProfessor, Department of Surgery, Section of Orthopedic Surgeryand Rehabilitation, University of Chicago

INTRODUCTION Section 2 of 11


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other divisions of muscles, the Nomina Anatomicareported by theInternational Anatomical Nomenclature Committee under the BerneConvention lists 200 paired muscles, or a total of 400 muscles. Anyone of these muscles can develop myofascial trigger points (TrPs)that refer pain and motor dysfunction, often to another location.

The myofascial pain syndromes (MPS) owe their ever-wideningacceptance to the pioneering work of Travell and her latercollaboration with Simons. In 1983, they combined their clinicalexperience in a detailed description of the multiple pain syndromesattributed to this disorder. In doing so, they further defined themajor clinical components that are characteristic of myofascial pain,the most important being the TrP, the taut band, and the localtwitch response.

Frequency:

In the US: Myofascial TrPs are extremely common andbecome a painful part of nearly everyone's life at one time oranother. Latent TrPs, which often cause motor dysfunction(eg, stiffness, restricted range of motion) without pain, are farmore common than active TrPs that cause pain.

Active TrPs are found commonly in postural muscles of theneck, shoulder, and pelvic girdles and in the masticatorymuscles. In addition, the upper trapezius, scalene,sternocleidomastoid, levator scapulae, and quadratuslumborum muscles are commonly involved.

Reports of the prevalence of myofascial TrPs in specificpatient populations are available. The data indicate a highprevalence of this condition among individuals with a regionalpain complaint, as shown in Table 1.

Table 1. Prevalence of Myofascial Pain

Region PracticeNumber

Studied

Prevalenceof

MyofascialPain, %

General Medical 172 30

GeneralPain medicalcenter

96 93

GeneralComprehensivepain center

283 85

Craniofacial

Head and neck

pain clinic 164 55




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The wide range in the prevalences of myofascial pain causedby 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 criteriaused to diagnose myofascial TrPs and, most important,differences in the training and skill of the examiners.

Functional Anatomy: Some isolated large round muscle fibersand some groups of these darkly staining, enlarged, round musclefibers appear in cross-sections. In longitudinal sections, thecorresponding feature is a number of contraction knots. Anindividual knot appears as a segment of muscle fiber with extremelycontracted sarcomeres. This contractured segment has a

corresponding increase in diameter of the muscle fiber.

The structural features of contraction knots presents a likelyexplanation for the palpable nodules and the taut bands associatedwith TrPs. Three single contraction knots can be seen scatteredamong normal muscle fibers. Beyond the thickened segment of thecontractured muscle fiber at the contraction knot, the muscle fiberbecomes markedly thinned and consists of stretched sarcomeres tocompensate for the contractured ones in the knot segment. Inaddition, a pair of contraction knots separated by emptysarcolemma may represent one of the first irreversible

complications that result from the continued presence of thecontraction knot.

Sport Specific Biomechanics: The activation of a TrP is usuallyassociated with some degree of mechanical abuse of the muscle inthe form of muscle overload, which may be acute, sustained, and/orrepetitive. In addition, leaving the muscle in a shortened positioncan convert a latent TrP to an active TrP; this process is greatlyaggravated if the muscle is contracted while in the shortenedposition.

In paraspinal muscles (and likely other muscles, too), a degree ofnerve compression that causes identifiable neuropathicelectromyographic (EMG) changes is associated with an increasein the numbers of active TrPs. These TrPs may be activated bydisturbed microtubular communication between the neuron and theendplate because the motor endplate is involved in thepathophysiologic process of the peripheral core TrP.

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

Distortion of the striations (sarcomere arrangement) inadjacent muscle fibers for some distance beyond the

LumboglutealOrthopedicclinic

97 21




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contraction knot (see Image 1). This produces unnaturalshear forces between fibers that could seriously andchronically stress the sarcolemma of the adjacent musclefibers. If the membrane were stressed to the point at which itbecame pervious to the relatively high concentration ofcalcium in the extracellular space, it could induce massive

contracture that could compound the shear forces.

The occasional finding of a segment of an empty sarcolemmaltube between 2 contractions knots may represent anadditional irreversible complication of a contraction knot.

Latent TrPs can produce other effects characteristic of a TrP,including increased muscle tension and muscle shortening; butthese do not produce spontaneous pain. Both active and latentTrPs can cause significant motor dysfunction. The same factorsthat are responsible for the development of an active TrP can, to a

lesser extent, cause a latent TrP. An active key TrP in one musclecan induce an active satellite TrP in another. Inactivation of the keyTrP often inactivates its satellite TrP without treatment of thesatellite TrP itself.

The intensity and extent of the pattern of referred pain depends onthe degree of irritability in the TrP, not on the size of the muscle.Myofascial TrPs in small, obscure, or variable muscles can be astroublesome 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 activatedindirectly by other existing TrPs, visceral disease, arthritic joints,joint dysfunctions, and emotional distress. Satellite TrPs are proneto develop in muscles that lie within the pain reference zone of keymyofascial TrPs or within the zone of pain referred from a diseasedviscus, such as the pain due to myocardial infarction, gastric ulcer,cholelithiasis, or renal colic. A perpetuating factor increases thelikelihood of overload stress that can convert a latent TrP to anactive TrP.

With adequate rest and in the absence of perpetuating factors, an

active TrP may spontaneously revert to a latent state. Painsymptoms disappear; however, occasional reactivation of the TrPby exceeding that muscles stress tolerance can account for ahistory of recurrent episodes of the same pain over a period ofyears.

History:

Symptoms

CLINICAL Section 3 of 11





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Active TrPs produce a clinical complaint, usually pain,that the patient recognizes when the TrP is compresseddigitally. The patient is aware of the pain caused by anactive TrP, but he or she may or may not be aware ofthe dysfunction it causes.

Latent TrPs characteristically cause increased muscletension and limit the stretch range of motion, whichoften escapes the patient's attention or is simplyaccepted. The patient becomes aware of painoriginating from a latent TrP only when pressure isapplied to it. Spontaneous referred pain appears withincreased irritability of the TrP; then, the TrP is identifiedas active.

The patient usually presents with complaints due to themost recently activated TrP. When this TrP is

successfully eliminated, the pain pattern may shift tothat of an earlier key TrP that must also be inactivated.If the key TrP is inactivated first, the patient may recoverwithout further treatment.

Patients with active myofascial TrPs usually complain ofpoorly localized, regional, aching pain in subcutaneoustissues, including muscles and joints. They rarelycomplain of sharp, clearly localized cutaneous-typepain. The myofascial pain is often referred away fromthe TrP in a pattern that is characteristic for each

muscle. Sometimes, the patient is aware of numbnessor paresthesia rather than pain.

Dysfunction

In addition to the clinical symptoms produced by thesensory disturbances of referred pain, dysesthesias,and hypesthesias, patients can also have clinicallyimportant disturbances of autonomic and motorfunctions.

Disturbances of autonomic functions

Disturbances of autonomic functions caused byTrPs include abnormal sweating, persistentlacrimation, persistent coryza, excessivesalivation, and pilomotor activities.

Related proprioceptive disturbances caused byTrPs include imbalance, dizziness, tinnitus, anddistorted perception of the weight of lifted objects.

Disturbances of motor functions

Disturbances of motor functions caused by TrPs




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include spasm of other muscles, weakness of theinvolved muscle function, loss of coordination bythe involved muscle, and decreased worktolerance of the involved muscle.

The weakness and loss of work tolerance are

often interpreted as an indication for increasedexercise, but if this is attempted withoutinactivating the responsible TrPs, the exercise islikely to encourage and further ingrain substitutionby other muscles, with further weakening anddeconditioning of the involved muscle.

The combination of weakness in the hands andloss of forearm muscle coordination makes thegrasp unreliable. Objects sometimes slipunexpectedly from the patient's grasp. The

weakness results from reflex motor inhibition andcharacteristically occurs without atrophy of theaffected muscle. Patients are prone to intuitivelysubstitute muscles without realizing that, forinstance, they are carrying the grocery bag in thenondominant but now stronger arm.

The motor effects of TrPs on the muscle in which theyare located are considered in detail under Surfaceelectromyography in Other Tests.

Sleep disturbances

Disturbance of sleep can be a problem for patients witha painful TrP syndrome. Authors of a series of studieshave shown that many sensory disturbances, includingpain, can seriously disturb the patients sleep.

This sleep disturbance can, in turn, increase painsensitivity the next day. Active myofascial TrPs becomemore painful when the muscle is held in the shortenedposition for long periods and if body weight compresses

the TrP. Thus, for patients with active TrPs, sleeppositioning can be critical to prevent unnecessarilydisturbances of their sleep.

Physical: Pain prevents a muscle with a TrP from reaching its fullstretch range of motion and also restricts its strength and/orendurance. Clinically, the lip is a localized spot of tenderness in anodule within a palpable taut band of muscle fibers. Restrictedstretch range of motion and a palpable increase in muscletenseness (ie, decreased compliance) are more severe in moreactive TrPs.

Active TrPs are identified when patients recognize the pain inducedby applying pressure to a TrP. The taut band fibers usually respond




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with a TrP when the taut band is accessible and when the TrP isstimulated by properly applied snapping palpation. The taut bandfibers have a consistent twitch response when a needle penetratesthe TrP.

Taut band

By gently rubbing across the direction of the musclefibers in a superficial muscle, the examiner can feel anodule at the TrP and a ropelike induration that extendsfrom this nodule to the attachment of the taut musclefibers at each end of the muscle.

The taut band can be snapped or rolled under the fingerin accessible muscles. With effective inactivation of theTrP, 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 noduleexhibiting a highly localized and exquisitely tender spotthat is characteristic of a TrP. When the spot is testedfor tenderness, displacement of the algometer by 2 cmproduces a statistically significant decrement in painthreshold algometer readings. Clinically, displacementof the application of pressure by 1-2 mm at a TrP can

result in a markedly reduced pain response.

This strong localization of tenderness in the vicinity of aTrP corresponds to the localized sensitivity of theexperimental muscle for eliciting TrPs as demonstratedin rabbit experiments. A 5-mm displacement to eitherside of the trigger spot (at right angles to the taut band)results in almost total loss of response. However, theresponse fades out more slowly when stimulated over arange of several centimeters from the trigger spot alongthe taut band.

Recognition: Application of digital pressure on either an activeor latent TrP can elicit a referred pain pattern characteristic ofthat muscle. However, if the patient recognizes the elicitedsensation as a familiar experience, this establishes the TrP asbeing active and is one of the most important diagnosticcriteria available when the palpable findings also are present.Similar recognition is observed frequently when a needlepenetrates 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 suchas tenderness and dysesthesias.




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Local twitch response: Snapping palpation of the TrPfrequently evokes a transient twitch response of the taut bandfibers. Twitch responses can be elicited both from active andlatent TrPs. Hubbard at al showed that no difference wasnoted in twitch responses whether elicited by snappingpalpation or by needle penetration. See Image 3.

Limited range of motion

Muscles with active myofascial TrPs have a restrictedpassive (stretch) range of motion because of pain. Anattempt to passively stretch the muscle beyond this limitproduces increasingly severe pain because the involvedmuscle fibers are already under substantially increasedtension at rest length.

The limitation of stretch due to pain is not as great with

active movement as with passive lengthening of themuscle; this finding at least partly due to reciprocalinhibition. When the TrP is inactivated and the taut bandis released, range of motion returns to normal.

The degree of limitation produced by TrPs is much moremarked in some muscles (eg, subscapularis) than inother muscles (eg, latissimus dorsi).

Painful contraction: When a muscle with an active TrP isstrongly contracted against fixed resistance, the patient feels

pain. This effect is most marked when the patient attempts tocontract the muscle when it is in a shortened position.

Weakness

Although weakness is generally characteristic of amuscle with active myofascial TrPs, the magnitude isvaries from muscle to muscle and from subject tosubject.

EMG studies indicate that, in muscles with active TrPs,

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 muscleby the TrPs.

Causes: Causes of myofascial pain include or are related to thefollowing:

The lack of motor unit action potentials due to theendogenous contracture of the contractile elements, ratherthan 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




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synaptic cleft region of an endplate

The release of substances that could sensitize nociceptors inthe region of the dysfunctional endplate of the TrP as a resultof tissue distress caused by the energy crisis

The effectiveness of essentially any technique that elongatesthe TrP portion of the muscle to its full stretch length evenbriefly, which could break the cycle that includes energy-consuming contractile activity

Laborers who exercise their muscles heavily every day areless likely to develop active TrPs than sedentary workers whoare prone to intermittent episodes of vigorous physicalactivity. This author's clinical experience supports thisobservation.

Ankle Impingement Syndrome

Other Problems to be Considered:

Fibromyalgia is fundamentally a different condition than TrPs, but it

often presents with symptoms that are confusingly similar to thosecaused by chronic myofascial TrPs. Fibromyalgia is characterizedby a central augmentation of nociception that causes generalizeddeep tissue tenderness that includes muscles. It has a differentetiology than myofascial TrPs, but many of the tender pointsdiagnostic of fibromyalgia also are common sites for TrPs andmany patients have both conditions. In the German literature,fibromyalgia usually is equated with generalized tendomyopathy(generalizierte tendomyopathie).

The term fibrositis appeared in the English literature in 1904 and

was soon adopted into German literature as the fibrositis syndrome.For most of the century, most authors characterized fibrositis as atender palpable fibrositic nodule. Many of these patients had TrPs.In time, fibrositis became an increasingly controversial diagnosisbecause of multiple definitions and no satisfactory histopathologicalbasis for the nodule. The diagnosis was completely redefined in1977, and the condition described by the 1977 definition wasofficially established in 1990 as fibromyalgia. According to thecurrent definition of fibromyalgia, it is a totally different conditionthat is unrelated to the original concept of fibrositis. Fibrositis iscurrently an outmoded diagnosis.

By 1921 the term muskelhartenwas well recognized in Germanliterature and still appears in German occasionally but rarely in

DIFFERENTIALS Section 4 of 11





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English. It literally means muscle indurations and refers to thepalpable firmness of the tender nodule responsible for the patient'spain. Another German term, myogelosen(literally muscle gellings)refers to the same phenomena, and the 2 terms frequently havebeen used interchangeably. The term muskelhartenoften is used tocharacterize the physical findings, and the term myogelosenis

used to identify the diagnosis.

This term myofascial pain syndrome has acquired both a generaland a specific meaning. The 2 meanings need to be distinguished.The general meaning includes a regional muscle pain syndrome ofany soft tissue origin that is associated with muscle tenderness andis commonly used in this sense by dentists. The other meaning isspecifically a myofascial pain syndrome caused by TrPs. This is afocal hyperirritability in muscle that can strongly modulate centralnervous system functions.

The term myofascitis is now rarely (and should not be) used assynonymous with myofascial TrPs. Myofascitis is properly used toidentify inflamed muscles.

The term myogeloses is the English form of a German term,myogelosen, which is still commonly used and is generallyconsidered synonymous with muskelharten. The name myogeloseswas based on an outmoded hypothesis to account for musclecontraction that was proposed before the actin-myosin contractilemechanism was discovered. A recent study indicates thatmyogeloses and TrPs identify the same condition approached from

somewhat different diagnostic points of view by using differentterminology.

Nonarticular rheumatism is a commonly used, but not very clearlydefined, general term for soft tissue pain syndromes that are notassociated with a specific joint dysfunction or disease. The termgenerally is considered as synonymous with soft tissuerheumatism, which is the English translation for the German termweichteilrheumatismus.

Weichteilrheumatismuswas commonly used to describe a range of

conditions that also include myofascial pain caused by TrPs.Currently, the term nonarticular rheumatism is used to identifymuscle pain syndromes that are not fibromyalgia and are notattributed to myofascial TrPs. The literature reviews of nonarticularrheumatism by Romano include conditions such as adhesivecapsulitis, periarticular arthritis, bursitis, epicondylitis, insertiontendinosis, and tennis elbow, which are frequently myofascial TrPsmasquerading as another diagnosis.

The term osteochondrosis is used by Russian vertebroneurologistsas an inclusive term to cover the interaction of neural and muscular

conditions, such as fibromyalgia, myofascial TrPs, and spinal nervecompromise.




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The term soft tissue rheumatism usually is used synonymously withnonarticular rheumatism.

Tendomyopathy is the English version of the German term that isdivided into general and local categories. General tendomyopathyis considered synonymous with fibromyalgia. The localized form

often includes myofascial TrPs but is not as clearly defined.

Overuse syndrome

In contrast to postexercise muscle pain, overuse muscle pain oftenoccurs in well-trained muscles. Overuse pain arises from therepetitive use of a muscle, not from a single bout of exercise. Theseinjuries are most common in athletes, musicians, and factory-lineworkers, where precise repetition of motor tasks is frequently arequirement for success.

The cause of overuse muscle pain is thought to be microtraumathat outpaces the capacity of the muscle for repair. Edwardsdescribes the final common pathway of muscle pain beginning withan excessive force per muscle fiber, leading to hypoxia, acidosis,and metabolic depletion, followed by calcium-mediated cellulardamage. In laborers, continued use of fatigued muscles causesmechanical damage that is directly related to the heaviness of thework. Again, eccentric work seems to subject small numbers ofmuscle fibers to excessive loads.

Many occupations require precise manipulations, leading to

excessive contraction of the proximal stabilizers that is unrelated tothe heaviness of the task. The forces required to perform the taskare not large enough to overload the muscles and cause damage.Rather, the conflict of motor control between the postural stabilizersand the muscles needed for precise manipulation or movementleads to the fiber damage.

The combination of mental stress and precise manipulationsexperienced by musicians/athletes can lead to occupational crampsbelieved to be of central origin (focal dystonia). These cramps maybe just an extreme example of the muscle pain that can occur with

disordered motor planning. They occur more commonly early in thecareer of the performer, before the smooth, seemingly effortlessmotor patterns are established.

Age

When children with musculoskeletal pain complaints wereexamined for myofascial TrPs, the TrPs were found to be acommon source of their pain. It gives the impression that thelikelihood of developing pain-producing active TrPs increases withage into the most active, middle years. As activity becomes less

strenuous in later years, individuals are more likely to be aware ofthe stiffness and restricted motion resulting from latent TrPs.




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Lab Studies:

No laboratory test or imaging technique is generally established as useful in thediagnosis of TrPs

Three measurable phenomena help to objectively substantiate the presenceof characteristic TrP phenomena, and all 3 are valuable as research tools.

Two of them, surface EMG and ultrasonography also have much potential forclinical application in the diagnosis and treatment of TrPs.

Imaging Studies:

In addition to EMG recording, ultrasonography provides a second way ofsubstantiating and studying the LTR and it also has a strong potential for providinga much needed available imaging technique that could be widely used toobjectively substantiate the clinical diagnosis of TrPs.

This test would require the examiner to use the skill-demanding snapping palpationtechnique, or to insert a needle into the TrP, to elicit the twitch response.

Other Tests:

Surface electromyography

TrPs cause distortion or disruption of normal muscle function.

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

With the recent appearance of online computer analysis of EMG

amplitude and mean power spectral frequency, a few pioneerinvestigators have reported the effects of TrPs on muscle activity. Thereports indicate that TrPs can influence the motor function of the musclein which they occur and that their influence can be transmitted throughthe central nervous system to other muscles.

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

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

Strong cutaneous stimuli (eg, electric shocks) are well known cause

WORKUP Section 5 of 11





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reflex motor effects (eg, flexion reflex). If the skin can modulate motoractivity and if TrPs can modulate sensory activity, the fact that TrPs canalso strongly affect motor activity should not be surprising. In fact, themotor effects of lips may be the most important influence they exert,because the motor dysfunction they produce may result in overload ofother muscles and spread the TrP problem from muscle to muscle.

Accumulating evidence now indicates that the muscles targeted forreferred spasm from TrPs also usually have TrPs themselves. Thesemotor phenomena of TrPs deserve serious competent researchinvestigation.

An increased responsiveness of some affected muscles is indicated byabnormally high amplitude of EMG activity when the muscle is voluntarilycontracted and loaded. Clinical evidence suggests that some muscles tend tobe shortened and abnormally excitable, while others appear to be weak andinhibited.

Fatigability noted at EMG and in terms of work tolerance, of the trapeziusmuscle that had myofascial TrPs is accelerated compared to a contralateralmuscle that was pain-free. The EMG amplitude increased and median powerfrequency decreased significantly in the involved muscle compared to theuninvolved muscle. Both of these changes are characteristic of initial fatigue.

Median power frequency generally is accepted as a valid criterion of musclefatigue. Delayed recovery following fatiguing exercise commonly is seen inpatients with muscle-related cumulative trauma disorder (CTD). MyofascialTrPs 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 repetitiveexercises of muscles with myofascial TrPs.

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

Algometry

Sensitivity to pain in patients with TrPs can be measured as the pain

threshold to electrical stimulation or applied pressure. The use of pressurealgometry is most commonly reported.

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

Most commonly, the pressure required to reach pain threshold is directlymeasured on a spring scale that is calibrated in kilograms, newtons, orrounds. Because the pressure is applied through a circular footplate, itsdiameter is a factor, and the actual measurement is stress (in kilograms persquare centimeter) applied to skin.




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For example, one of the most common algometers has a footplate area of 1

cm2; therefore, its meter, which provides readings in kilograms, is numericallythe same as the number of kilograms per square centimeter, and no numericconversion is needed.

Thermography

Thermograms can be recorded by using infrared radiometry or films of liquidcrystal. Recording infrared radiation (ie, electronic thermography) withcomputer analysis provides a powerful tool for tile accurate rapid visualizationof skin temperature changes over large areas of the body. This technique candemonstrate cutaneous reflex phenomena characteristic of myofascial TrPs.The less expensive contact sheets of liquid crystal have limitations that makereliable 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 changescorrespond to changes in the circulation within, but not beneath, the skin. Theendogenous cause of these temperature changes is usually sympatheticnervous system activity. Therefore, thermographic changes in skintemperature are comparable in meaning to changes in skin resistance orchanges in sweat production. However, electronic infrared thermography issuperior to these other two measures (ie, infrared radiometry or with films ofliquid crystal) in convenience and in spatial as well as temporal resolution.

In summary, Fishers research studies indicate that the finding a hot spot onthe 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 hotspot of a TrP is described as a discoid region 5 to 1 (3 cm in diameter,displaced slightly from directly over the TrP).

Procedures:

Procedures to confirm diagnose of MPS: The first international symposium onmyofascial pain and fibromyalgia was held in 1989. It marked one of the firstmeetings of the principal proponents of the 2 major muscle pain syndromes. In theproceedings of that symposium, Simons listed the clinical criteria for diagnosis of

MPS.

Clinical criteria for the diagnosis of MPS caused by active TrPs

To make the clinical diagnosis of MPS, the findings should include 5 majorcriteria and at least 1 of 3 minor criteria. The 5 major criteria include thefollowing:

Regional pain complaint

Pain complaint or altered sensation in the expected distribution of

referred pain from a myofascial TrP

Taut band palpable in an accessible muscle




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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, bypressure on the tender spot

Elicitations of a local twitch response by transverse snapping palpationat the tender spot or by needle insertion into the tender spot in the tautband

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

Additional symptoms, such as weather sensitivity, sleep disturbance, anddepression, often are present, but they are not diagnostic because they maybe attributable to chronic, severe pain perpetuated by multiple mechanicaland/or systemic perpetuating factors.

The required features include regional pain, referred pain, or disturbed sensation ina predicted location; a taut band; a tender point along the taut band; and restrictedrange 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. Toqualify, the point must be exquisitely tender, located in a taut band of a muscle withrestricted range of motion, refer pain when pressed or needled, and exhibit a twitchresponse when needled.

Acute Phase:

Rehabilitation Program:

Physical Therapy: Effective treatment of a MPS caused by TrPs usuallyinvolves more than simply applying a procedure to TrPs. Often, it is necessaryto consider and deal with the cause that activated the TrPs, to identify and

correct any perpetuating factors (which often are different than what activatedthe TrPs), and to help the patient to restore and maintain normal musclefunction. Common misconceptions about the treatment of TrPs include the

TREATMENT Section 6 of 11





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following:

Simply treating the TrP should be sufficient, especially if the stress thatactivated the TrP is not recurrent and if no perpetuating factors arepresent. Otherwise, the TrP is likely to be reactivated by the samestress. Ignoring perpetuating factors invites recurrence. After the TrPs

have persisted for some time, failure to retrain the muscle to normalfunction or failure to reestablish its full-stretch range of motion results ina degree of persistent motor dysfunction.

The pain cannot be as severe as the patient says and must be largelypsychogenic. The patients are trying to communicate their degree ofpain. Believe them. The pain feels severe to them. Patients in a generalmedical practice rated their pain as severe as or more severe than painfrom other causes such as pharyngitis, cystitis, angina, and herpeszoster.

In addition, an appreciable amount of the pain reported by manypatients with fibromyalgia comes from their TrPs. The pain offibromyalgia rates fully as severe as the pain of rheumatoid arthritis. It issevere enough to cause central nervous system changes characteristicof chronic pain.

Because of their chronic lip and fibromyalgia pain, these patients oftendevelop pain behaviors that tend to reinforce dysfunction and furtherpain. Many patients experience grievous and needless degree andduration of pain, because a series of clinicians unacquainted withmyofascial TrPs erroneously (covertly if not overtly) diagnosed a

psychogenic condition.

MPSs are self-limiting and will cure themselves. An acuteuncomplicated TrP activated by an unusual activity or muscle overloadcan revert spontaneously to a latent TrP within 1 or 2 weeks, if themuscle is not overstressed (used within tolerance, which may be limited)and if no perpetuating factors are present. Otherwise, if the acutesyndrome is not properly managed, it evolves needlessly into a chronicMPS.

Relief of pain by treatment of skeletal muscles for myofascial TrPs rules

out serious visceral disease. Because of the referred pain nature ofvisceral pain, application of Vapo coolant spray or infiltration of a localanesthetic into the somatic reference zone can temporarily relieve thepain of myocardial infarction, angina, and acute abdominal disease withno effect on the visceral pathology.

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

Physical therapy includes simple muscle stretch, augmented muscle stretch,post-isometric relaxation, reciprocal inhibition, slow exhalation, eye




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movement, TrP pressure release, massage, range of motion, heat,ultrasound, and high-voltage galvanic stimulation.

Medical Issues/Complications:

Table 2. Myofascial TrPs Mistakenly Diagnosed as Other Conditions

Initial Diagnosis TrPs

Angina pectoris, atypical Pectoralis major

Appendicitis Lower rectus abdominis

Atypical facial neuralgiaMasseter, temporalis, sternal division of thesternocleidomastoid, upper trapezius

Atypical migraine Sternocleidomastoid, temporalis, posteriorcervical

Back pain, middle Upper rectus abdominis, thoracic paraspinals

Back pain, lowLower rectus abdominis, thoracolumbarparaspinals

Bicipital tendinitis Long head of the biceps brachii

Chronic abdominal wall

pain

Abdominal muscles

Dysmenorrhea Lower rectus abdominis

Earache, enigmatic Deep masseter

Epicondylitis Wrist extensors, supinator, triceps brachii

Frozen shoulder Subscapularis

Myofascial pain

dysfunction

Masticatory muscles

Occipital headache Posterior cervicals

Post-therapeuticneuralgia

Serratus anterior, intercostals

Radiculopathy, C6 Pectoralis minor, scalenes

Scapulocostal syndrome Scalenes, middle trapezius, levator scapulae

Subacromial bursitis Middle deltoid

Temporomandibular joint




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Table 3. Differences in Clinical Features that Distinguish Myofascial Pain due toTrPs from Fibromyalgia

Complications of injections

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

The location of the needle tip can be misjudged readily when a long,slender needle is used. Furthermore, the needle should be insertedstraight to prevent avoid any side pressure that might bend it and deflectthe tip an unknown distance to one side.

The location of the needle tip can be misjudged readily when using along slender needle. Furthermore, the needle should be insertedstraight, avoiding any side pressure that might bend it, deflecting the tip

disorder Masseter, lateral pterygoid

Tennis elbow Finger extensors, supinator

Tension headacheSternocleidomastoid, masticatory, posterior

cervicals, suboccipital, upper trapezius

Thoracic outlet syndromeScalenes, subscapularis, pectoralis minor andmajor, latissimus dorsi, teres major

FeatureMyofascial

Pain

(TrPs)

Fibromyalgia

Female-to-male ratio

1:1 4-9:1

PainLocal orregional

Widespread,general

Tenderness Focal Widespread

Muscle

Feels

tense (tautbands)

Feels softand doughy

MotionRestrictedrange ofmotion

Hypermobility

ExaminationExaminefor TrPs

Examine fortender points




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an unknown distance to one side.

It is especially important to avoid using a needle with a burr at the tipbecause it causes unnecessary bleeding. When the tip of a disposableneedle contacts bone, the impact frequently curls the tip to produce afishhook burr that feels scratchy and drags as the needle is drawnthrough tissues.

Contraindications to TrP injections

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 atleast 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 myofascial TrPs to practitioners has

been described in the literature for acupuncturists, anesthesiologists, chronic painmanagers, dentists, family practitioners, gynecologists, neurologists, nurses,orthopedic surgeons, pediatricians, physical therapists, physiatrists,rheumatologists, and veterinarians.

Other Treatment (injection, manipulation, etc.): Infants have been observed with

point tenderness of the rectus abdominis muscle and colic, both of which wererelieved by sweeping a stream of Vapo coolant over the muscle, which helps toinactivate myofascial TrPs.

The clinical effectiveness of botulinum A toxin injection for the treatment ofmyofascial TrPs helps to substantiate dysfunctional endplates as an essential partof the pathophysiology of TrPs (see Image 10). This toxin specifically acts only onthe neuromuscular junction, effectively denervating that muscle cell.

Sequence of steps when stretching and spraying any muscle for myofascialTrPs (see Image 4)

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 overthe length of the muscle in the direction of pain pattern.

After the first sweep of spray, pressure is applied to take up the slack inthe 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




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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 Image5).

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

Unidirectional sweeps cover, first, parallel lines of skin over thosemuscle fibers that are stretched the tightest, then over the rest of the

muscle and its pain pattern. Sequential sweeps of spray should followthe direction of the muscle fibers and progress toward the referred painzone.

TrP injection

To prevent bleeding, the fingers of the palpating hand should be spreadapart, maintaining tension on the skin to reduce the likelihood ofsubcutaneous bleeding where the needle has penetrated (see Image 7).Also, during the injection, the fingers exert pressure around the needletip to provide homeostasis in deeper tissues. When the angle of the

needle is changed, the direction of pressure changes.

The physician should avoid inserting the needle to the hub where theneedle is most likely to break off. Some additional depth of penetrationcan be obtained safely by indenting the skin and subcutaneous tissueswith a finger beside the needle as illustrated in Image 8.

The importance of distinguishing between central TrPs, ie, in the centralportion of the muscle belly and attachment TrPs when injecting, isillustrated in Image 9.

The increased capillary fragility characteristic of a low serum vitamin C levelcan cause excessive bleeding in muscles injected for TrPs. Capillaryhemorrhage augments postinjection soreness and leads to unsightlyecchymoses. A frequent source of increased bleeding due to low vitamin C istobacco. Mega-dose vitamin C therapy daily for 1 week should correct thisdeficiency. At least 500 mg of timed-release vitamin C 3 times daily isrecommended for a minimum of 3 days prior to injection of TrPs. A daily doseof aspirin increases the susceptibility to bleeding. The patient should take noaspirin for 3 days before TrP injection or needling.

Recovery phase:





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Physical Therapy: See Acute Phase Physical Therapy.

Occupational Therapy: See Acute Phase Physical Therapy.

Other Treatment (injection, manipulation, etc.):

Maintenance Phase:


Physical Therapy: See above

Anti-inflammatory agents, including corticosteroids and analgesics, are generally notuseful, and their administration should be avoided. Localized and regional muscle painsyndromes often respond to specific localized therapies. The most common treatment forlocalized muscle pain is injection. Take great care in locating the TrP, watch for the twitchresponse on the muscle, and then enter the muscle with the needle.

Drug Category: Local anesthetics-- Amide derivative local anesthetic used tominimize postinjection soreness.

MEDICATION Section 7 of 11


Drug Name

Lidocaine HCL (Xylocaine) -- Has rapid onset

of action. Stabilizes neuronal membrane byinhibiting the sodium flux required for theinitiation and conduction of impulses. Inaddition, causes inhibition of release ofneurotransmitters (eg, substance P), ATPfrom nociceptive afferent C fibers, modulationin information transfer along primaryafferents, and central sympathetic blockadewith decrease in pain-induced reflexvasoconstriction.

Adult Dose

1% solution without vasoconstrictor: 0.2 mL

SC per TrP 2 times/wk until symptomsdisappear (usually within 3 wk)

Pediatric Dose Not established

Contraindications Documented hypersensitivity

Interactions

May potentiate the neuromuscular blockingeffect of succinylcholine, tubocurarine;reduced clearance with concomitant use ofbeta-blocking agents, cimetidine;benzodiazepines, barbiturates, and volatileanesthetics increase seizure threshold;

duration of regional anesthesia prolonged byvasoconstrictor agents; alkalinizationincreases rate of onset and potency of local




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or regional anesthesia

PregnancyB - Usually safe but benefits must outweighthe risks.

Precautions

Caution in patients with hypovolemia, severecongestive heart failure, shock, and all forms

of heart block; adverse reactions includehypotension, bradycardia, arrhythmias,respiratory depression, tinnitus, seizures,loss of hearing, euphoria, anxiety, diplopia,palsies, urticaria, pruritus, angioneuroticedema

Drug Name

Procaine HCL 0.5% solution (Novocaine) --Procaine HCL 0.5% solution (Novocaine) --Regional anesthesia for treatment of painfulconditions (eg, neuropathic pain, reflexsympathetic dystrophy, myofascial pain).Least myotonic and has lowest systemictoxicity among commonly used localanesthetics. Procaine is the ester of p-aminobenzoic acid and ethanol with a tertiarydiethylamino group attached at the other endof the alcohol. Stabilizes neuronal membraneand prevents the initiation and transmissionof impulses. Has a rapid onset of action andrelatively short duration depending onanesthetic technique, type of block,concentration, and patient. Greater solutionconcentration does not increase anestheticeffect.

Adult Dose0.2 mL SC per TrP 2 times/wk untilsymptoms disappear (usually within 3 wk);not to exceed 1 g per injection


Contraindications

Documented hypersensitivity to procaine orester-type local anesthetics and in individualswith allergy to suntan lotion, which containsPABA derivatives

Interactions

Prolongs the effect of succinylcholine;metabolite (PABA) inhibits action ofsulfonamides and aminosalicylic acid;benzodiazepines, barbiturates, and volatileanesthetics increase seizure threshold;duration of regional anesthesia prolonged byvasoconstrictor agents (eg, epinephrine) andalpha 2-agonists (eg, clonidine);alkalinization increases rate of onset andpotency of local or regional anesthesia

Pregnancy B - Usually safe but benefits must outweighthe risks.

Do not use vasoconstrictor drugs for this kind




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Drug Category: Neurotoxins-- Botulinum toxin type A (BTA) binds irreversibly topresynaptic cholinergic nerve terminals, which includes the terminals of motor nervesupplying skeletal muscle-fiber endplates. Since the primary dysfunction of motorendplates associated with the TrP phenomenon appears to be excessive release ofacetylcholine (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 theneuromuscular junction, effectively denervating that muscle cell. See Picture 10 throughPicture 15 for the mechanism of action of BTA.

Precautions

of regional anesthesia because of risk ofmuscle damage, including necrosis; cautionin patients with severe disturbances ofcardiac rhythm or heart block; reduce dosesin obstetric, elderly, hypovolemic, and high-risk patients; bacteriostatic agent commonly

added to procaine is sodium bisulphite, whichcan be irritating and contribute topostinjection soreness (can reduced thiseffect by diluting 2% procaine solution to0.5% with isotonic sodium chloride solution)

Drug Name

Botulinum toxin type A (Botox) -- BTA blocksneuromuscular transmission through a 3-stepprocess, as follows: (1) blockade ofneuromuscular transmission; BTA binds tothe motor nerve terminal. The bindingdomain of the type A molecule appears to bethe heavy chain, which is selective forcholinergic nerve terminals. (2) BTA isinternalized via receptor-mediatedendocytosis, a process in which the plasmamembrane of the nerve cell invaginatesaround the toxin-receptor complex, forming atoxin-containing vesicle inside the nerveterminal. After internalization, the light chainof the toxin molecule, which has beendemonstrated to contain the transmission-blocking domain, is released into thecytoplasm of the nerve terminal. (3) BTAblocks acetylcholine release by cleaving

SNAP-25, a cytoplasmic protein that islocated on the cell membrane and that isrequired for the release of this transmitter.The affected terminals are inhibited fromstimulating muscle contraction. The toxindoes not affect the synthesis or storage ofacetylcholine or theconduction of electrical signals along thenerve fiber.Typically, a 24-72 h delay betweenadministration of toxin and onset of clinical

effects exists, which terminate in 2-6 mo.This purified neurotoxin complex is avacuum-dried form of purified BTA, which




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contains 5 ng of neurotoxin complex proteinper 100 U.BTA has to be reconstituted with 2 mL of0.9% sodium chloride diluent. With thissolution each 0.1 mL results in 5 U dose.Patient should receive 5-10 injections per

visit.

Adult Dose

5-10 U of BTA per TrP (0.1-0.2 mL), not toexceed 90 U; recurrent injections, ifnecessary to inactivate the TrP, should begiven after 8 wk


Contraindications

Patients with myasthenia gravis or othermuscular endplate disorders; adverse effectsassociated with BTA usually transient andmild to moderate and may include drooping

of the eyelid, eye irritation, dry eye, tearing orlight sensitivity (in patients treated forblepharospasm), and superficial punctatekeratitis at injection site

Interactions

With >92 U of BTA over 6 wk, effectivenessmay be reduced due to antibody production;effects of BTA therapy may be increased withthe use of aminoglycoside antibiotics or otherdrugs that interfere with neuromusculartransmission

Pregnancy C - Safety for use during pregnancy has notbeen established.

Precautions

High doses, frequent injections, andexposure to neurotoxin complex proteins areall thought to play important roles in theformation of neutralizing antibodies, whichmay lead to nonresponse or resistance;using neurotoxins with a low protein load, thelowest effective dose, and the longestinterval between injections may help tominimize the potential for antibody formation;

axon sprouting and muscle fiberreinnervation terminate the clinical toxiceffect of BTA, which results in thereestablishment of neuromusculartransmissionChemical denervation of the neuromuscularjunction by BTA results in an expansion ofthe endplate region and growth stimulation ofcollateral axonal sprouts; a nerve sprouteventually establishes a new neuromuscularjunction, and muscle activity gradually

returns; however, new research suggeststhat this new nerve sprout retracts and theoriginal junction returns to functionality; in




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Return to Play: The athlete should avoid strenuous activity during sports, and theyshould always use stretching techniques prior to competitions or practice.

Complications: The single muscle MPSs usually are acute and follow an episode ofmuscle 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 painproblem. Mechanical factors include postural stress, muscle imbalances, and skeletalasymmetries. These can put additional stress on surrounding muscles, leading to spreadof dysfunction and pain. Systemic perpetuating factors purportedly include anythingjeopardizing the energy supply to muscle (ie, anemia, endocrine imbalances, low thyroidfunction, vitamin deficiencies).

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

Prevention: Patients should avoid the mechanical and systemic factors mentioned inComplications.

Education: The ultimate goal is to educate patients and (1) to provide them with themeans to manage their own muscle pain disorder, (2) to eliminate their dependence onhealthcare providers, (3) to eliminate contributing factors, providing prolonged stretch ofthe affected muscle, and aerobic exercises.

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

Medical/Legal Pitfalls:

As with most diagnoses in medicine, the most important aspect is a completehistory and careful physical examination, in this case emphasizing the

musculoskeletal and neurologic components.

Points to remember include the following:

either case, repeat injections may berequired to maintain the desired clinical effectIntramuscular injections of BTA typicallyresult in a dose-dependent reduction ofhyperactive muscle contraction that lasts for

approximately 3 mo and is ultimatelyreversible

FOLLOW-UP Section 8 of 11


MISCELLANEOUS Section 9 of 11





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Pain is within or over muscles or their attachments not in the joints.

Results of the neurologic examination, including sensation, and reflexes arenormal. However, strength is usually weak and joint examination is oftenrestricted.

Laboratory findings are within normal limits.

Special Concerns:

Flat palpation is used to locate the TrP for injection, its position can be confirmedprecisely by pushing the nodular TrP back and forth between 2 fingers (see Image6).

Then, the TrP can be fixed for injection by pinning it down midway between thefingertips (see Image 6). This identifies the plane that passes through the TrPperpendicular to the skin. The needle can be aimed half way between the fingers

precisely in that plane and angled to whatever depth is necessary to reach the TrP.

PICTURES Section 10 of 11


Caption: Picture 1. Myofascial pain in athletes. Schematic of a trigger pointcomplex of a muscle in longitudinal section.

A, The central trigger point (CTrP) in the endplate zone contains numerouselectrically active loci and numerous contraction knots. A taut band of muscle fibersextends 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 caninduce 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. Thesarcomeres within one of these enlarged segments (ie, contraction knot) of amuscle fiber are markedly shorter and wider than the sarcomeres in the neighboringnormal muscle fibers, which are free of contraction knots.

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Caption: Picture 2. Myofascial pain in athletes. Cross-sectional drawing shows flatpalpation of a taut band and its trigger point.

Left, Skin pushed to one side to begin palpation (A). The fingertip slides acrossmuscle fibers to feel the cord-line texture of the taut band rolling beneath it (B). Theskin 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). Thehardness of the taut band is felt clearly as it is rolled between the digits (B). Thepalpable edge of the taut band is sharply defined as it escapes from between thefingertips, often with a local twitch response (C).



Picture Type: Image

Caption: Picture 3. Myofascial pain in athletes. Longitudinal schematic drawing oftaut bands, myofascial trigger points, and a local twitch response. A, Palpation of ataut band (straight lines) among normally slack, relaxed muscle fibers (wavy lines).

B, Rolling the band quickly under the fingertip (snapping palpation) at the triggerpoint often produces a local twitch response that usually is seen most clearly asskin movement between the trigger point and the attachment of the muscle fibers.



Picture Type: Image

Caption: Picture 4. Myofascial pain in athletes. Sequence of steps to use whenstretching and spraying any muscle for myofascial trigger points.





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Picture Type: Image

Caption: Picture 5. Myofascial pain in athletes. Schematic drawing showing howthe jet stream of Vapo coolant is applied.



Picture Type: Image

Caption: Picture 6. Myofascial pain in athletes. Cross-sectional schematic drawingshows flat palpation to localize and hold the trigger point for injection. A and B showuse of alternate pressure between 2 fingers to confirm the location of the palpablemodule of the trigger point. C shows positioning the trigger point half way betweenthe fingertips to keep it from sliding to one side during the injection.


eMedicine Zoom View (Interactive!)

Picture Type: Image

Caption: Picture 7. Myofascial pain in athletes. Schematic top view of 2approaches 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).





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Picture Type: Image

Caption: Picture 8. Myofascial pain in athletes. C. Z. Hongs technique. Fingerpressure beside the needle is used to indent the skin, subcutaneous, and fattissues so that the needle can reach the trigger point in a muscle that would beinaccessible otherwise.



Picture Type: Image

Caption: Picture 9. Myofascial pain in athletes. Diagrammatic representation of

pre-injection sites (open circles) and injection sites (solid circles) of local anestheticto the trigger point. The enclosed stippled area represents the taut band. Thisdiagram distinguishes the central trigger point within the large broken circle from theattachment trigger points located at the myotendinous junction and at theattachment of the tendon to the bone. Each of these 3 trigger point regions can beidentified by their individual spot tenderness and anatomical locations. No rationaleis apparent for injecting the part of the taut band that lies between the central triggerpoint and the attachment trigger point (solid circles numbers 7-10).



Picture Type: Image

Caption: Picture 10. Myofascial pain in athletes. Mechanism of botulinum toxin typeA.




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Picture Type: Image

Caption: Picture 11. Myofascial pain in athletes. Binding of neuromusculartransmission with botulinum toxin type A, which binds the motor nerve terminal.



Picture Type: Image

Caption: Picture 12. Myofascial pain in athletes. After botulinum toxin type A isinternalized, the light chain of the toxin molecule is released into the cytoplasm ofthe nerve terminal.


eMedicine Zoom View

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Picture Type: Image

Caption: Picture 13. Myofascial pain in athletes. Botulinum toxin type A blocksacetylcholine by cleaving a cytoplasmic protein on the cell membrane.


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Acquadro MA, Borodic GE: Treatment of myofascial pain with botulinum A toxin.

(Interactive!)

Picture Type: Image

Caption: Picture 14. Myofascial pain in athletes. After the botulinum toxin type Aexerts its clinical toxic effect, a nerve sprout eventually establishes a newneuromuscular junction, and muscle activity gradually returns. However, newresearch findings suggest that this new nerve sprout retracts and the original

junction returns to functionality.



Picture Type: Image

Caption: Picture 15. Myofascial pain in athletes. After the clinical toxic effect ofbotulinum toxin type A occurs, axon sprouting and muscle fiber reinnervationterminate the clinical effect of the toxin, which results in the reestablishment ofneuromuscular transmission.



Picture Type: Image

BIBLIOGRAPHY Section 11 of 11





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Anesthesiology 1994 Mar; 80(3): 705-6[Medline]. Charness ME, Parry GJ, Markison RE, et al: Entrapment neuropathies in

musicians. Neurology 1985; 35(suppl 1): 74. Cheshire WP, Abashian SW, Mann JD: Botulinum toxin in the treatment of

myofascial pain syndrome. Pain 1994 Oct; 59(1): 65-9[Medline]. Coffield JA, Considine RV, Simpson LL: The site and mechanism of action of

botulinum neurotoxin. In: Jankovic J, Hallet M, eds. Therapy with Botulinum Toxin.New York, NY: Marcel Dekker, Inc; 1994: 3-13.

Fisher AA: Diagnosis and management of chronic pain in physical medicine andrehabilitation. In Ruskin AP, ed. Current Therapy in Physiatry. Philadelphia, Pa:W.D. Saunders; 1984: 123-54.

Hatheway CL, Dang C: Immunogenicity of the neurotoxins of Clostridium botulinum.In: Jankovic J, Hallet M, eds. Therapy with Botulinum Toxin. New York, NY: MarcelDekker, Inc; 1994: 93-107.

Hubbard DR, Berkoff GM: Myofascial trigger points show spontaneous needle EMGactivity. Spine 1993 Oct 1; 18(13): 1803-7[Medline].

Lambert CM: Hand and upper limb problems of instrumental musicians. Br J

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nerve in violin players. J Neurol Neurosurg Psychiatry 1991 Jan; 54(1): 65-7[Medline].

Reiter RC, Gambone JC: Nongynecologic somatic pathology in women with chronicpelvic pain and negative laparoscopy. J Reprod Med 1991 Apr; 36(4): 253-9[Medline].

Rosen NB: Myofascial pain: the great mimicker and potentiator of other diseases inthe performing artist. Md Med J 1993 Mar; 42(3): 261-6[Medline].

Schneider MJ: Tender points/fibromyalgia vs. trigger points/myofascial painsyndrome: a need for clarity in terminology and differential diagnosis. JManipulative Physiol Ther 1995 Jul-Aug; 18(6): 398-406[Medline].

Scott AB: Forward. In: Jankovic J, Hallet M, eds. Therapy with Botulinum Toxin.New York, NY: Marcel Dekker, Inc; 1994: VII-IX.

Simons AG: Muscular pain syndromes. In: Fricton JR, Awad FA, eds. Advances inPain Research and Therapy. Myofascial Pain and Fibromyalgia. Vol 17. New York,NY: Raven Press; 1990: 18.

Thompson JM: The diagnosis and treatment of muscle pain syndromes. In:Braddom RL, ed. Physical Medicine and Rehabilitation. Philadelphia, Pa: WBSaunders Co; 1996.

Travell JG, Simons DG: Myofascial Pain and Dysfunction: The Trigger PointManual. Baltimore, Md: Lippincott Williams & Wilkins; 1983. Travell JG: Ethylchloride spray for painful muscle spasm. Arch Phys Med Rehabil

1952; 33: 291-8. Travell JG, Simons DG: Myofascial Pain and Dysfunction: The Trigger Point

Manual. Vol 1. Upper half of Body. 2nd ed. Baltimore, Md: Williams & Wilkins; 1999. Wainapel SF, Cole IL: The not so magic flute: two cases of distal ullnar nerve

entrapment. Med Probl Perform Art 1988; 3: 63-5. Walsh NE, Dimitru D, Schoenfeld LS, Ramamurthy S: Treatment of the patient with

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NOTE:

Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment




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therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date andaccurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changingand human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article donot warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for theresults of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, alldrug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

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