myofascial trigger points: an evidence-informed review - david g

The Journal of Manual & Manipulative TherapyVol. 14 No. 4 (2006), 203 - 221 Myofascial Trigger Points: An Evidence-Informed Review / 203

Myofascial Trigger points: an evidence-informed review

Addressallcorrespondenceandrequestforreprintsto:JanDommerholtBethesdaPhysiocare,Inc.7830OldGeorgetownRoad,SuiteC-15Bethesda,[email protected]

Abstract:Thisarticleprovidesabestevidence-informedreviewofthecurrentscientificun-derstandingofmyofascialtriggerpointswithregardtotheiretiology,pathophysiology,andclinicalimplications.Evidence-informedmanualtherapyintegratesthebestavailablescien-tificevidencewithindividualclinicians’judgments,expertise,andclinicaldecision-making.Afterabriefhistoricalreview,theclinicalaspectsofmyofascialtriggerpoints,theinterraterreliability for identifying myofascial trigger points, and several characteristic features arediscussed, including the taut band, local twitch response, and referred pain patterns. Theetiologyofmyofascialtriggerpointsisdiscussedwithadetailedandcomprehensivereviewofthemostcommonmechanisms,includinglow-levelmusclecontractions,unevenintramus-cularpressuredistribution,direct trauma,unaccustomedeccentriccontractions,eccentriccontractionsinunconditionedmuscle,andmaximalorsub-maximalconcentriccontractions.Manycurrentscientificstudiesareincludedandprovidesupportforconsideringmyofascialtriggerpointsintheclinicaldecision-makingprocess.Thearticleconcludeswithasummaryoffrequentlyencounteredprecipitatingandperpetuatingmechanical,nutritional,metabolic,andpsychologicalfactorsrelevantforphysicaltherapypractice.Currentscientificevidencestronglysupportsthatawarenessandworkingknowledgeofmuscledysfunctionandinpar-ticularmyofascialtriggerpointsshouldbeincorporatedintomanualphysicaltherapypracticeconsistentwiththeguidelinesforclinicalpracticedevelopedbytheInternationalFederationofOrthopaedicManipulativeTherapists.Whiletherearestillmanyunansweredquestionsinexplainingtheetiologyofmyofascial triggerpoints, thisarticleprovidesmanualtherapistswithanup-to-dateevidence-informedreviewofthecurrentscientificknowledge.

Key Words : Myofascia l Pain Syndrome, Tr igger Points , Myofascia l , Et io logy,Pathophysiology

Jan Dommerholt, PT, MPS, FAAPMCarel Bron, PTJo Franssen, PT

Duringthepastfewdecades,myofascialtriggerpoints(MTrPs)andmyofascialpainsyndrome(MPS)have

received much attention in the scientific and clinicalliterature. Researchers worldwide are investigatingvariousaspectsofMTrPs,includingtheirspecificetiol-ogy,pathophysiology,histology,referredpainpatterns,and clinical applications. Guidelines developed by theInternational Federation of Orthopaedic Manipulative

Therapists (IFOMT)confirmthe importanceofmuscledysfunctionfororthopedicmanualtherapyclinicalprac-tice.TheIFOMThasdefinedorthopedicmanualtherapyas“aspecializedareaofphysiotherapy/physicaltherapyfor the management of neuromusculoskeletal condi-tions,basedonclinicalreasoning,usinghighlyspecifictreatmentapproachesincludingmanualtechniquesandtherapeutic exercises.” The educational standards ofIFOMTrequirethatskillswillbedemonstratedin—amongothers—“analysisandspecifictestsforfunctionalstatusofthemuscularsystem,”“ahighlevelofskill inothermanual and physical therapy techniques required tomobilizethearticular,muscularorneuralsystems,”and“knowledgeofvariousmanipulativetherapyapproachesaspracticedwithinphysicaltherapy,medicine,osteopathyandchiropractic”1.

204 / The Journal of Manual & Manipulative Therapy, 2006

However, articles aboutmuscledysfunction in themanualtherapyliteraturearesparseandtheygenerallyfocusonmuscleinjuryandmusclerepairmechanisms2oronmusclerecruitment3.Untilveryrecently,thecurrentscientificknowledgeandclinicalimplicationsofMTrPswererarelyincluded4-7.Itappearsthatorthopedicmanualtherapistshavenot paidmuchattention to thepatho-physiologyandclinicalmanifestationsofMTrPs.ManualtherapyeducationalprogramsintheUSseemtoreflectthisorientationandtendtoplaceastrongemphasisonjointdysfunction,mobilizations,andmanipulationswithonlyabout10%-15%ofclassroomeducationdevotedtomusclepainandmuscledysfunction.

This review of the MTrP literature is based oncurrent best scientific evidence. The field of manualtherapyhasjoinedothermedicaldisciplinesbyembrac-ing evidence-based medicine, which proposes that theresultsofscientificresearchneedtobeintegratedintoclinical practice8. Evidence-based medicine has beendefined as “the conscientious, explicit, and judicioususeofcurrentbestevidenceinmakingdecisionsaboutthecareofindividualpatients”9,10.Withintheevidence-basedmedicineparadigm,evidence isnotrestrictedtorandomized controlled trials, systematic reviews, andmeta-analyses,althoughthisrestrictedviewseemstobeprevalentinthemedicalandphysicaltherapyliterature.Sackettetal9,10emphasizedthatexternalclinicalevidencecaninformbutnotreplaceindividualclinicalexpertise.Clinicalexpertisedetermineswhetherexternalclinicalevidenceappliestoanindividualpatient,andifso,howit should be integrated into clinical decision-making.Pencheon11 shared this perspective and suggested thathigh-quality healthcare is about combining “wisdomproducedbyyearsofexperience”with“evidenceproducedbygeneralizableresearch”in“wayswithwhichpatientsarehappy.”Hesuggestedshifting fromevidence-basedtoevidence-informedmedicine,whereclinicaldecision-makingisinformedbyresearchevidencebutnotdrivenby it and always includes knowledge from experience.Evidence-informed manual therapy involves integrat-ing thebest available external scientific evidencewithindividual clinicians’ judgments, expertise, and clini-caldecision-making12.Thepurposeof thisarticle is toprovideabestevidence-informedreviewofthecurrentscientificunderstandingofMTrPs,includingtheetiology,pathophysiology, and clinical implications, against thebackgroundofextensiveclinicalexperience.

brief Historical reviewWhileDr.JanetTravell(1901-1997)isgenerallycred-

ited forbringingMTrPstotheattentionofhealthcareproviders,MTrPshavebeendescribedandrediscoveredforseveralcenturiesbyvariouscliniciansandresearchers13,14.Asfarbackasthe16thcentury,deBaillou(1538-1616),ascitedbyRuhmann,describedwhat isnowknownasmyofascial pain syndrome (MPS)15. MPS is defined as

the “sensory, motor, and autonomic symptoms causedbyMTrPs”andhasbecomea recognizedmedicaldiag-nosisamongpainspecialists16,17.In1816,Britishphysi-cianBalfour,ascitedbyStockman,described“nodulartumorsandthickeningswhichwerepainfultothetouch,and from which pains shot to neighboring parts”18. In1898, the German physician Strauss discussed “small,tenderandapple-sizednodulesandpainful,pencil-sizedtolittle-finger-sizedpalpablebands”19.Thefirsttriggerpointmanualwaspublishedin1931inGermanynearlya decade before Travell became interested in MTrPs20.Whiletheseearlydescriptionsmayappearabitarchaicandunusual—forexample,inclinicalpracticeonedoesnotencounter“apple-sizednodules”—theseandotherhistoricpapersdidillustratethebasicfeaturesofMTrPsquiteaccurately14.

In the late 1930s, Travell, who at that time was acardiologistandmedicalresearcher,becameparticularlyinterested in muscle pain following the publication ofseveralarticlesonreferredpain21.Kellgren’sdescriptionsof referred pain patterns of many muscles and spinalligamentsafter injectingthese tissueswithhypertonicsaline22-25eventuallymovedTravelltoshifthermedicalcareerfromcardiologytomusculoskeletalpain.Duringthe 1940s, she published several articles on injectiontechniques of MTrPs26-28. In 1952, she described themyofascial genesis of pain with detailed referred painpatternsfor32muscles29.OthercliniciansalsobecameinterestedinMTrPs.EuropeanphysiciansLiefandChaitowdevelopedatreatmentmethod,whichtheyreferredtoas“neuromusculartechnique”30.GermanphysicianGutsteindescribedthecharacteristicsofMTrPsandeffectivemanualtherapy treatments in several papers under the namesofGutstein,Gutstein-Good,andGood31-34.InAustralia,Kellyproducedaseriesofarticlesaboutfibrositis,whichparalleledTravel’swritings35-38.

In the US, chiropractors Nimmo and Vannerson39describedmuscular“noxiousgenerativepoints,”whichwerethoughttoproducenerveimpulsesandeventuallyresultin“vasoconstriction,ischaemia,hypoxia,pain,andcellulardegeneration.”Laterinhiscareer,Nimmoadoptedthe term “trigger point” after having been introducedtoTravell’swritings.Nimmomaintainedthathypertonicmusclesarealwayspainfultopressure,astatementthatlater became known as “Nimmo’s law.” Like Travell,Nimmodescribeddistinctivereferredpainpatternsandrecommended releasing these dysfunctional points byapplyingtheproperdegreeofmanualpressure.Nimmo’s“receptor-tonuscontrolmethod”continuestobepopularamongchiropracticphysicians39,40.Accordingtoa1993reportbytheNationalBoardofChiropracticEconomics,over 40% of chiropractors in the US frequently applyNimmo’s techniques41. Two spin-offs of Nimmo’s workareSt.JohnNeuromuscularTherapy(NMT)methodandNMTAmericanversion,whichhavebecomeparticularlypopularamongmassagetherapists30.

Myofascial Trigger Points: An Evidence-Informed Review / 205

In1966,TravellfoundedtheNorthAmericanAcademyofManipulativeMedicine,togetherwithDr.JohnMennell,who also published several articles about MTrPs42,43. Throughout her career Travell promoted integratingmyofascial treatmentswitharticular treatments16.Oneof her earlier papers described a technique for reduc-ingsacroiliacdisplacement44.However,Travell,ascitedby Paris45, maintained the opinion that manipulationswere the exclusive domain of physicians and she re-jectedmembership in theNorthAmericanAcademyofManipulativeMedicinebyphysicaltherapists.

Intheearly1960s,Dr.DavidSimonswasintroducedto Travell and her work, which became the start of afruitfulcollaborationeventuallyresultinginseveralpub-lications,includingtheTrigger Point Manuals,consist-ingofa1983firstvolume(upperhalfofthebody)anda1992secondvolume(lowerhalfofthebody)46,47.Thefirst volumehas sincebeen revisedandupdatedandasecondeditionwasreleasedin199916.TheTrigger Point Manuals are the most comprehensive review of nearly150 muscle referred-pain patterns based on Travell’sclinical observations, and they include an extensivereview of the scientific basis of MTrPs. Both volumeshave been translated into several foreign languages,including Russian, German, French, Italian, Japanese,and Spanish. Several other clinicians worldwide havealsopublishedtheirowntriggerpointmanuals48-54.

clinical aspects of Myofascial Trigger points

An MTrP is described as “a hyperirritable spot inskeletalmusclethatisassociatedwithahypersensitivepalpablenoduleinatautband”16.Myofascialtriggerpointsareclassifiedintoactiveandlatenttriggerpoints16.AnactiveMTrPisasymptom-producingMTrPandcantriggerlocal or referred pain or other paraesthesiae. A latentMTrP does not trigger pain without being stimulated.Myofascialtriggerpointsarethehallmarkcharacteris-ticsofMPSandfeaturemotor,sensory,andautonomiccomponents. Motor aspects of active and latent MTrPsmay include disturbed motor function, muscle weak-ness as a result of motor inhibition, muscle stiffness,andrestrictedrangeofmotion55,56.Sensoryaspectsmayinclude local tenderness, referral of pain to a distantsite,andperipheralandcentralsensitization.Peripheralsensitizationcanbedescribedasareductioninthresholdandanincreaseinresponsivenessoftheperipheralendsofnociceptors,whilecentralsensitizationisanincreaseintheexcitabilityofneuronswithinthecentralnervoussystem.Signsofperipheralandcentralsensitizationareallodynia(painduetoastimulusthatdoesnotnormallyprovokepain)andhyperalgesia (an increased responsetoastimulusthatisnormallypainful).BothactiveandlatentMTrPsarepainfuloncompression.Vecchietetal57-

59describedspecificsensorychangesoverMTrPs.They

observedsignificantloweringofthepainthresholdoveractiveMTrPswhenmeasuredbyelectricalstimulation,notonlyinthemusculartissuebutalsointheoverlyingcutaneous and subcutaneous tissues. In contrast,withlatent MTrPs, the sensory changes did not involve thecutaneousandsubcutaneoustissues57-59.AutonomicaspectsofMTrPsmayinclude,amongothers,vasoconstriction,vasodilatation, lacrimation,andpiloerection16,60-63.

Adetailedclinicalhistory,examinationofmovementpatterns,andconsiderationofmusclereferred-painpat-terns assist clinicians in determining which musclesmay harbor clinically relevant MTrPs64. Muscle pain isperceivedasachingandpoorly localized.TherearenolaboratoryorimagingtestsavailablethatcanconfirmthepresenceofMTrPs.Myofascialtriggerpointsareidenti-fiedthrougheitheraflatpalpationtechnique(Figure1)in which a clinician applies finger or thumb pressureto muscle against underlying bone tissue, or a pincerpalpation technique (Figure 2) in which a particularmuscleispalpatedbetweentheclinician’sfingers.

Fig.1: Flat palpation

Fig.2: Pincer palpation


Bydefinition,MTrPsarelocatedwithinatautbandofcontracturedmusclefibers(Figure3),andpalpatingforMTrPsstartswithidentifyingthistautbandbypalpatingperpendiculartothefiberdirection.Oncethetautbandis located, the clinician moves along the taut band to

guides the clinician. The presence of a so-called localtwitchresponse(LTR),referredpain,orreproductionofthe person’s symptomatic pain increases the certaintyand specificity of the diagnosis of MPS. Local twitchresponses are spinal reflexes that appear to be uniquetoMTrPs.Theyarecharacterizedbyasuddencontrac-tionofmusclefiberswithinatautband,whenthetautband is strummed manually or needled. The suddencontractionscanbeobservedvisually, canbe recordedelectromyographically, or can be visualized with diag-nostic ultrasound72. When an MTrP is needled with amonopolar teflon-coated EMG needle, LTRs appear ashigh-amplitudepoly-phasicEMGdischarges73-78.

In clinical practice, there is no benefit in usingneedleEMGorsonography,anditsutilityislimitedtoresearchstudies.Forexample,Audetteetal79establishedthatin61.5%ofactiveMTrPsinthetrapeziusandlevatorscapulaemuscles,dryneedlinganactiveMTrPelicitedanLTRinthesamemuscleontheoppositesideofthebody. Needling of latent MTrPs resulted in unilateralLTRs only. In this study, LTRs were used to researchthe nature of active versus latent MTrPs. Studies haveshownthatclinicaloutcomesaresignificantlyimprovedwhenLTRsareelicitedinthetreatmentofpatientswithdry needling or injection therapy74,80,81. The taut band,MTrP,andLTR(Figure4)areobjectivecriteria,identifiedsolelybypalpation,thatdonotrequireaverbalresponsefromthepatient82.

Active MTrPs refer pain usually to a distant site.Thereferredpainpatterns(Figure5)arenotnecessarily

Fig. 3: Palpation of a trigger point within a taut band (reproduced with permission from Weisskircher H-W. Head Pains Due to Myofascial Trigger Points. CD-ROM, www.trigger-point.com, 1997)

findadiscreteareaof intensepainandhardness.Two studies have reported good overall interrater

reliabilityforidentifyingtautbands,MTrPs,referredpain,and local twitch responses65,66. The minimum criteriathatmustbe satisfied inorder todistinguishanMTrPfrom any other tender area in muscle are a taut bandandatenderpoint inthattautband65.AlthoughJandamaintained that systematic palpation can differentiatebetweenmyofascialtautbandsandgeneralmusclespasms,electromyographyisthegoldstandardtodifferentiatetautbandsfromcontractedmusclefibers67,68.Spasmscanbedefinedaselectromyographic(EMG)activityastheresultof increasedneuromusculartoneof theentiremuscle,andtheyaretheresultofnerve-initiatedcontractions.Atautbandisanendogenouslocalizedcontracturewithinthemusclewithoutactivationof themotorendplate69.Fromaphysiologicalperspective,theterm“contracture”ismoreappropriatethen“contraction”whendescribingchronic involuntary shortening of a muscle withoutEMGactivity. Inclinicalpractice,surfaceEMGisusedinthediagnosisandmanagementofMTrPsinadditionto manual examinations67,70,71. Diagnostically, surfaceEMGcanassistinassessingmusclebehaviorduringrestand during functional tasks. Clinicians use the MTrPreferred pain patterns in determining which musclesto examine with surface EMG. Muscles that harborMTrPs responsible for thepatient’spaincomplaintareexamined first. EMG assessments guide the clinicianwith postural training, ergonomic interventions, andmuscleawarenesstraining67.

Thepatient’srecognitionoftheelicitedpainfurther

Fig. 4: Local twitch response in a rabbit trigger spot. Local twitch responses are elicited only when the needle is placed accurately within the trigger spot. Moving as little as 0.5 cm away from the trigger spot virtually eliminates the local twitch response (reproduced with permission from Hong C-Z, Torigoe Y. Electrophysiological characteristics of localized twitch responses in responsive taut bands of rabbit skeletal muscle. J Musculoskeletal Pain 1994;2:17-43)


restricted to single segmental pathways or to periph-eralnervedistributions.Althoughtypicalreferredpainpatterns have been established, there is considerablevariationbetweenpatients16,48.

Usually, the pain in reference zones is described as“deeptissuepain”ofadullandachingnature.Occasion-ally,patientsmayreportburningortinglingsensations,especially in superficial muscles such as the platysmamuscle83,84. By mechanically stimulating active MTrPs,patientsmayreportthereproductionoftheirpain,eitherimmediately or after a 10-15 second delay. Normally,skeletal muscle nociceptors require high intensities ofstimulation and they do not respond to moderate localpressure, contractions, or muscle stretches85. However,MTrPscausepersistentnoxiousstimulation,whichresultsinincreasingthenumberandsizeofthereceptivefieldstowhichasingledorsalhornnociceptiveneuronresponds,and the experience of spontaneous and referred pain86.Several recent studies have determined previously un-recordedreferredpainpatternsofdifferentmusclesandMTrPs87-90.Referredpain isnotspecific toMPSbut it isrelativelyeasytoelicitoverMTrPs91.Normalmuscletissueandotherbodytissues,includingtheskin,zygapophysealjoints,orinternalorgans,mayalsoreferpaintodistantregionswithmechanicalpressure,makingreferredpainelicitedbystimulationofatenderlocationanonspecificfinding84,92-95.Gibsonetal96foundthatreferredpainisactu-allyeasiertoelicitintendon-bonejunctionsandtendonthan in the muscle belly. However, after exposing themuscletoeccentricexercise,significantlyhigherreferredpainfrequencyandenlargedpainareaswerefoundatthemusclebellyandthetendon-bonejunctionsitesfollowinginjection with hypotonic saline. The authors suggestedthat central sensitizationmay explain the referredpain

frequencyandenlargedpainareas97.While a survey of members of the American Pain

SocietyshowedgeneralagreementthatMTrPsandMPSexist as distinct clinical entities, MPS continues to beone of the most commonly missed diagnoses17,98. In arecentstudyof110adultswithlowbackpain,myofascialpain was the most common finding affecting 95.5% ofpatients,eventhoughmyofascialpainwaspoorlydefinedasmusclepainintheparaspinalmuscles,piriformis,ortensorfasciaelatae99.Astudyofadultswithfrequentmi-graineheadachesdiagnosedaccordingtotheInternationalHeadacheSocietycriteriashowedthat94%ofthepatientsreported migrainous pain with manual stimulation ofcervicalandtemporalMTrPs,comparedwithonly29%ofcontrols100,101.In30%ofthemigrainegroup,palpationofMTrPseliciteda“full-blownmigraineattackthatrequiredabortive treatment.” The researchers found a positiverelationshipbetween thenumberofMTrPsand the fre-quencyofmigraineattacksanddurationoftheillness100.SeveralstudieshaveconfirmedthatMTrPsarecommonnotonly inpersonsattendingpainmanagementclinicsbutalsointhoseseekinghelpthroughinternalmedicineand dentistry102-107. In fact, MTrPs have been identifiedwithnearlyeverymusculoskeletalpainproblem,includ-ing radiculopathies104, joint dysfunction108, disk pathol-ogy109, tendonitis110, craniomandibular dysfunction111-113,migraines100,114,tension-typeheadaches7,87,carpaltunnelsyndrome115,computer-relateddisorders116,whiplash-as-sociated disorders60,117, spinal dysfunction118, and pelvicpainandotherurologicsyndromes119-122.Myofascialtriggerpointsareassociatedwithmanyotherpainsyndromes123,including,forexample,post-herpeticneuralgia124,125,complexregionalpainsyndrome126,127,nocturnalcramps128,phantompain129,130,andotherrelativelyuncommondiagnosessuchasBarré-Liéousyndrome131andneurogenicpruritus132.ArecentstudysuggestedthattheremightbearelationshipbetweenMTrPsintheuppertrapeziusmuscleandcervicalspinedysfunctionat theC3andC4vertebrae,althougha cause-and-effect relationship was not established inthiscorrelational study133.Anotherstudydescribed thatpersons with mechanical neck pain had significantlymore clinically relevant MTrPs in the upper trapezius,sternocleidomastoid, levator scapulae, and suboccipitalmusclesascomparedtohealthycontrols5.

etiology of MTrpsSeveralpossiblemechanismscanleadtothedevel-

opmentofMTrPs, including low-levelmuscle contrac-tions,unevenintramuscularpressuredistribution,directtrauma,unaccustomedeccentriccontractions,eccentriccontractionsinunconditionedmuscle,andmaximalorsubmaximalconcentriccontractions.

Low-levelmusclecontractionsOf particular interest in the etiology of MTrPs are

low-levelmuscleexertionsandtheso-calledCinderella

Fig.5: MTrP referred pain patterns (reproduced with per-mission from MEDICLIP, Manual Medicine 1 & 2, Version 1.0a, 1997, Williams & Wilkins)


HypothesisdevelopedbyHäggin1988134.TheCinderellaHypothesispostulatesthatoccupationalmyalgiaiscausedby selective overloading of the earliest recruited andlastde-recruitedmotorunitsaccordingtotheorderedrecruitmentprincipleorHenneman’s“sizeprinciple”134,135.Smallermotorunitsarerecruitedbeforeandde-recruitedafterlargerones;asaresult,thesmallertype1fibersarecontinuouslyactivatedduringprolongedmotortasks135.AccordingtotheCinderellaHypothesis,muscularforcegeneratedatsub-maximallevelsduringsustainedmusclecontractionsengagesonlyafractionofthemotorunitsavailablewithoutthenormallyoccurringsubstitutionofmotorunitsduringhigherforcecontractions,whichinturncanresultinmetabolicallyoverloadedmotorunits,prone to loss of cellular Ca2+-homeostasis, subsequentactivationofautogenicdestructiveprocesses,andmusclepain136,137.TheotherpillaroftheCinderellaHypothesisisthefindingofanexcessofraggedredfibersinmyalgicpatients136.Indeed,severalresearchershavedemonstratedthepresenceofraggedredfibersandmoth-eatenfibersinsubjectswithmyalgia,whichareindicationsofstruc-tural damage to the cell membrane and mitochondriaandachangeinthedistributionofmitochondriaorthesarcotubularsystemrespectively138-142.

Thereisgrowingevidencethatlow-levelstaticmusclecontractionsorexertionscanresultindegenerationofmuscle fibers143. Gissell144,145 has shown that low-levelexertions can result in an increase of Ca2+-release inskeletalmusclecells,musclemembranedamageduetoleakageoftheintracellularenzymelactatedehydrogenase,structuraldamage,energydepletion,andmyalgia.Low-levelmusclestimulationcanalsoleadtothereleaseofinterleukin6(IL-6)andothercytokines146,147.

SeveralstudieshaveconfirmedtheCinderellaHy-pothesis and support the idea that in low-level staticexertions, muscle fiber recruitment patterns tend tobe stereotypicalwithcontinuousactivationof smallertype 1 fibers during prolonged motor tasks148-152. AsHäggindicated,thecontinuousactivityandmetabolicoverload of certain motor units does not occur in allsubjects136. The Cinderella Hypothesis was recentlyapplied to the development of MTrPs116. In a well-de-signedstudy,Treastersetal116establishedthatsustainedlow-levelmusclecontractionsduringcontinuoustypingfor as little as 30 minutes commonly resulted in theformationofMTrPs.TheysuggestedthatMTrPsmightprovideausefulexplanationformusclepainandinjurythatcanoccur fromlow-level staticexertions116.Myo-fascial trigger points are common in office workers,musicians, dentists, and other occupational groupsexposed to low-level muscle exertions153. Chen et al154also suggested that low-level muscle exertions canleadtosensitizationanddevelopmentofMTrPs.Fortypiano students showed significantly reduced pressurethresholdsover latentMTrPsafteronly20minutesofcontinuouspianoplaying154.

IntramuscularpressuredistributionOtten155hassuggestedthatcirculatorydisturbances

secondarytoincreasedintramuscularpressuremayalsoleadtothedevelopmentofmyalgia.Basedonmathemati-cal modeling applied to a frog gastrocnemius muscle,Otten confirmed that during static low-level musclecontractions, capillary pressures increase dramaticallyespeciallynearthemuscleinsertions(Figure6).Inotherwords, during low-level exertions, the intramuscular

Fig.6: Intramuscular pressure distribution in the gastroc-nemius muscle of the toad (reproduced with permission from E. Otten, 2006)

pressure near the muscle insertions might increaserapidly,leadingtoexcessivecapillarypressure,decreasedcirculation,andlocalizedhypoxiaandischaemia155.Withhigher level contractions in between 10% and 20% ofmaximumvoluntaryeffort,theintramuscularpressureincreases also in the muscle belly156,157. According toOtten,theincreasedpressuregradientsduringlow-levelexertionsmaycontributetothedevelopmentofpainatthemusculotendinous junctions and eventually to theformationofMTrPs(personalcommunication,2005).

In1999,Simonsintroducedtheconceptof“attach-menttriggerpoints”toexplainpainatthemusculoten-dinous junctions in persons with MTrPs, based on theassumption that taut bands would generate sufficientsustained forceto induce localizedenthesopathies16,158.Morerecently,Simonsconcludedthatthereisnocon-vincingevidencethatthetensiongeneratedinshortenedsarcomeres in a muscle belly would indeed be able togeneratepassiveorresting force throughoutanentiretaut band resulting in enthesopathies, even though


theremaybecertainmusclesorconditionswherethiscould occur (personal communication, 2005). To thecontrary, force generated by individual motor units isalwaystransmittedlaterallytothemuscle’sconnectivetissuematrix, involvingatleasttwoproteincomplexescontainingvinculinanddystrophin,respectively159.Thereis alsoconsiderable evidence that theassumption thatmuscle fibers pass from tendon to tendon is withoutbasis160.Trotter160hasdemonstratedthatskeletalmuscleiscomprisedofin-seriesfibers.Inotherwords,thereisevidence that a single muscle fiber does not run fromtendon to tendon. The majority of fibers are in serieswithinactivefibers,whichmakesitevenmoreunlikelythatthewholemusclelength-tensionpropertieswouldbe dictated by the shortest contractured fibers in themuscle161.

Inaddition,itisimportanttoconsiderthemechanicalandfunctionaldifferencesbetweenfastandslowmotorunits162,163.Slowmotorunitsarealwaysstifferthanfastunits, although fast units can produce more force. Iftherewereanytransmissionof forcealongthemusclefiber,asSimonsinitiallysuggested,fastfiberswouldbebetter suited to accomplish this. Yet, fast motor unitshave larger series of elastic elements, which wouldabsorbmostof the forcedisplacement164,165.Fast fibersshowaprogressivedecreaseincross-sectionalareaandendinapointwithinthemusclefascicle,makingforcetransmissionevenmoreunlikely163.Fast fibers relyontransmitting a substantial proportion of their force tothe endomysium, transverse cytoskeleton, and adja-cent muscle fibers162,163. In summary, the developmentof so-called “attachment trigger points” as a result ofincreasedtensionbycontracturedsarcomeresinMTrPsisnotclearandmoreresearchisneededtoexplaintheclinical observation that MTrPs appear to be linked topain at the musculotendinous junction. The increasedtensioninthemusclebellyis likelytodissipateacrossbriefsectionsofthetautbandonbothsidesoftheMTrPand laterally through the transversecytoskeleton166-168.Instead,Otten’smodelofincreasedintramuscularpressure,decreasedcirculation,localizedhypoxia,andischaemiaatthemuscleinsertionsprovidesanalternativemodelfortheclinicallyobservedpainnearthemusculotendinousjunctionandosseousinsertionsinpersonswithMTrPs,eventhoughthemodeldoesnotexplainwhytautbandsarecommonlypresent155.

DirecttraumaThereisgeneralagreementthatacutemuscleover-

load can activate MTrPs, although systematic studiesarelacking169.Forexample,peopleinvolvedinwhiplashinjuries commonly experience prolonged muscle painanddysfunction170-173. Ina retrospective review,Schul-leretal174foundthat80%of1096subjectsinvolvedinlow-velocitycollisionsdemonstratedevidenceofmusclepain with myogeloses among the most common find-

ings. Although Schuller et al174 did not define thesemyogeloses, Simons has suggested that a myogelosisdescribesthesameclinicalentityasanMTrP175.Baker117reported that thespleniuscapitis, semispinaliscapitis,andsternocleidomastoidmusclesdevelopedsymptomaticMTrPs in77%,62%,and52%of52whiplashpatients,respectively.Inaretrospectivereviewof54consecutivechronic whiplash patients, Gerwin and Dommerholt176reported that clinically relevant MTrPs were found ineverypatient,withthetrapeziusmuscleinvolvedmostoften.FollowingtreatmentemphasizingtheinactivationofMTrPsandrestorationofnormalmusclelength,ap-proximately80%ofpatientsexperiencedlittleornopain,even though the average time following the initiatinginjurywas2.5yearsat thebeginningof the treatmentregimen.Allpatientshadbeenseenpreviouslybyotherphysicians and physical therapists who apparently hadnot considered MTrPs in their thought process andclinicalmanagement176.Fernández-de-las-Peñasetal177,178confirmedthatinactivationofMTrPsshouldbeincludedinthemanagementofpersonssufferingfromwhiplash-associateddisorders.Intheirresearch-basedtreatmentprotocol,thecombinationofcervicalandthoracicspinemanipulations with MTrP treatments proved superiorto more conventional physical therapy consisting ofmassage, ultrasound, home exercises, and low-energyhigh-frequencypulsedelectromagnetictherapy177.

Directtraumamaycreateaviciouscycleofeventswherein damage to the sarcoplasmic reticulum or themuscle cell membrane may lead to an increase of thecalciumconcentration,asubsequentactivationofactinandmyosin,arelativeshortageofadenosinetriphosphate(ATP), and an impaired calcium pump, which in turnwill increase the intracellular calcium concentrationevenmore,completingthecycle.Thecalciumpumpisresponsible for returning intracellular Ca2+ to the sar-coplasmic reticulum against a concentration gradient,whichrequiresafunctionalenergysupply.SimonsandTravell179 considered this sequence in thedevelopmentof the so-called “energy crisis hypothesis” introducedin 1981. Sensory and motor system dysfunction havebeenshowntodeveloprapidlyafterinjuryandactuallymaypersist in thosewhodevelopchronicmusclepainand in individuals who have recovered or continue tohave persistent mild symptoms172,180. Scott et al181 de-termined that individuals with chronic whiplash paindevelopmorewidespreadhypersensitivitytomechanicalpressure and thermal stimuli than those with chronicidiopathic neck pain. Myofascial trigger points are alikely source of ongoing peripheral nociceptive input,and they contribute to both peripheral and centralsensitization, which may explain the observation ofwidespreadallodyniaandhypersensitivity60,62,63.Inaddi-tion to being caused by whiplash injury, acute muscleoverloadcanoccurwithdirect impact, lifting injuries,sportsperformance,etc.182.


Eccentricand(sub)maximalconcentriccontractionsManypatientsreporttheonsetofpainandactivation

of MTrPs following either acute, repetitive, or chronicmuscleoverload183.Gerwinetal184suggestedthatlikelymechanisms relevant for the development of MTrPsincluded either unaccustomed eccentric exercise, ec-centric exercise in unconditioned muscle, or maximalor sub-maximal concentric exercise. A brief review ofpertinentaspectsofexercisefollows,precedinglinkingthisbodyofresearchtocurrentMTrPresearch.

Eccentricexerciseisassociatedwithmyalgia,muscleweakness, and destruction of muscle fibers, partiallybecause eccentric contractions cause an irregular andunevenlengtheningofmusclefibers185-187.Musclesore-ness and pain occur because of local ultra-structuraldamage,thereleaseofsensitizingalgogenicsubstances,and the subsequent onset of peripheral and centralsensitization85,188-190.Muscledamageoccursatthecyto-skeletallevelandfrequentlyinvolvesdisorganizationoftheA-band,streamingoftheZ-band,anddisruptionofcytoskeletalproteins,suchastitin,nebulin,anddesmin,evenafterveryshortboutsofeccentricexercise186,189-194.Lossofdesmincanoccurwithin5minutesofeccentricloading,eveninmusclesthatroutinelycontracteccen-tricallyduringfunctionalactivities,butdoesnotoccurafter isometric or concentric contractions193,195. Lieberand Fridén193 suggested that the rapid loss of desminmightindicateatypeofenzymatichydrolysisorproteinphosphorylationasalikelymechanism.

Oneoftheconsequencesofmuscledamageismuscleweakness196-198. Furthermore, concentric and eccentriccontractions are linked to contraction-induced capil-laryconstrictions, impairedbloodflow,hypoperfusion,ischaemia, and hypoxia, which in turn contribute tothedevelopmentofmoremuscledamage,alocalacidicmilieu,andanexcessivereleaseofprotons(H+),potassium(K+),calcitonin-gene-related-peptide(CGRP),bradykinin(BK),andsubstanceP(SP),andsensitizationofmusclenociceptors184,188. There are striking similarities withthe chemical environment of active MTrPs establishedwith microdialysis, suggesting an overlap between theresearchoneccentricexerciseandMTrPresearch184,199.However,atthistime,itisprematuretoconcludethatthereissolidevidencethateccentricandsub-maximalconcentric exercise are absolute precursors to the de-velopment of MTrPs. In support of this hypothesizedcausal relation, Itoh et al200 demonstrated in a recentstudythateccentricexercisecanleadtotheformationoftautandtenderropybandsinexercisedmuscle,andtheyhypothesizedthateccentricexercisemayindeedbeausefulmodelforthedevelopmentofMTrPs.

Eccentric and concentric exercise andMTrPshavebeen associated with localized hypoxia, which appearsto be one of the most important precursors for thedevelopment of MTrPs201. As mentioned, hypoxia leadstothereleaseofmultiplealgogenicsubstances.Inthis

context, recentresearchbyShahetal199at theUSNa-tionalInstitutesofHealthisparticularlyrelevant.Shahetalanalyzed thechemicalmilieuof latentandactiveMTrPsandnormalmuscles.Theyfoundsignificantlyin-creasedconcentrationsofBK,CGRP,SP,tumornecrosisfactor-α(TNF-α),interleukin-1β(IL-1β),serotonin,andnorepinephrineintheimmediatemilieuofactiveMTrPsonly199.Thesesubstancesarewell-knownstimulantsforvariousmusclenociceptorsandbindtospecificreceptormoleculesofthenerveendings,includingtheso-calledpurinergicandvanilloidreceptors85,202.

Muscle nociceptors are dynamic structures whosereceptors can change depending on the local tissueenvironment. When a muscle is damaged, it releasesATP, which stimulates purinergic receptors, which aresensitivetoATP,adenosinediphosphate,andadenosine.TheybindATP,stimulatemusclenociceptors,andcausepain.VanilloidreceptorsaresensitivetoheatandrespondtoanincreaseinH+-concentration,whichisespeciallyrelevant under conditions with a lowered pH, such asischaemia, inflammation, or prolonged and exhaustivemusclecontractions85.Shahetal199determinedthatthepH at active MTrP sites is significantly lower than atlatentMTrPsites.AloweredpHcaninitiateandmain-tainmusclepainandmechanicalhyperalgesiathroughactivationofacid-sensingionchannels203,204.Neuroplasticchanges in the central nervous system facilitate me-chanical hyperalgesia even after the nociceptive inputhas been terminated (central sensitization)203,204. Anynoxiousstimulussufficienttocausenociceptoractiva-tioncausesburstsofSPandCGRPtobe released intothemuscle,whichhaveasignificanteffectonthelocalbiochemicalmilieuandmicrocirculationbystimulating“feed-forward” neurogenic inflammation. Neurogenicinflammationcanbedescribedasacontinuouscycleofincreasing production of inflammatory mediators andneuropeptidesandanincreasingbarrageofnociceptiveinput into wide dynamic-range neurons in the spinalcorddorsalhorn184.

The integrated Trigger point HypothesisThe integrated triggerpointhypothesis (Figure7)

has evolved since its first introduction as the “energycrisishypothesis”in1981.Itisbasedonacombinationofelectrodiagnosticandhistopathologicalevidence179,183.

Alreadyin1957,WeeksandTravell205hadpublisheda report that outlined a characteristic electrical activ-ity of an MTrP. It was not until 1993 that Hubbard etal206 confirmed that this EMG discharge consists oflow-amplitudedischargesintheorderof10-50µVandintermittenthigh-amplitudedischarges(upto500µV)in painful MTrPs. Initially, the electrical activity wastermed “spontaneous electrical activity” (SEA) andthoughttoberelatedtodysfunctionalmusclespindles206.BestavailableevidencenowsuggeststhattheSEAisinfact endplate noise (EPN), which is found much more


commonlyintheendplatezonenearMTrPsthaninanendplatezoneoutsideMTrPs207-209.Theelectricaldischargesoccurwith frequencies thatare10-1,000 times thatofnormalendplatepotentials,andtheyhavebeenfoundinhumans,rabbits,andrecentlyeven inhorses209,210.Thedischarges aremost likely the result of an abnormallyexcessive release of acetylcholine (ACh) and indicativeofdysfunctionalmotorendplates,contrarytothecom-monlyacceptednotionamongelectromyographersthatendplate noise arises from normal motor endplates183.The effectiveness of botulinum toxin in the treatmentofMTrPsprovides indirect evidenceof thepresenceofexcessiveACh211.Botulinumtoxin(BoTox)isaneurotoxinthatblocksthereleaseofAChfrompresynapticcholiner-gicnerveendings.Arecentstudyinmicedemonstratedthattheadministrationofbotulinumtoxinresultedinacompletefunctionalrepairofdysfunctionalendplates212.ThereissomeearlyevidencethatmusclestretchingandhypertonicitymayalsoenhancetheexcessivereleaseofACh213,214. Tension on the integrins in the presynapticmembraneatthemotornerveterminalishypothesizedto mechanically trigger an ACh release that does notrequireCa2+213-215.Integrinsarereceptorproteinsinthecellmembraneinvolvedinattachingindividualcellstotheextracellularmatrix.

Excessive ACh affects voltage-gated sodium chan-nels of the sarcoplasmic reticulum and increases theintracellular calcium levels, which triggers sustainedmuscle contractures. It is conceivable that in MTrPs,myosin filaments literally get stuck in the Z-band ofthe sarcomere. During sarcomere contractions, titinfilaments are folded into a gel-like structure at the Z-band.InMTrPs,thegel-liketitinmaypreventthemyosinfilaments from detaching. The myosin filaments mayactuallydamagetheregularmotorassemblyandprevent

thesarcomerefromrestoringitsrestinglength216.MusclecontracturesarealsomaintainedbecauseoftherelativeshortageofATPinanMTrP,asATPisrequiredtobreakthecross-bridgesbetweenactinandmyosin filaments.The question remains whether sustained contracturesrequireanincreaseofoxygenavailability.

Atthesametime,theshortenedsarcomerescompro-misethelocalcirculationcausingischaemia.StudiesofoxygensaturationlevelshavedemonstratedseverehypoxiainMTrPs201.Hypoxia leads to thereleaseof sensitizingsubstancesandactivatesmusclenociceptorsasreviewedabove.Thecombineddecreasedenergysupplyandpos-sible increased metabolic demand would also explainthe common finding of abnormal mitochondria in thenerveterminalandthepreviouslymentionedraggedredfibers.Inmice,theonsetofhypoxialedtoanimmediateincreasedAChreleaseatthemotorendplate217.

Thecombinedhigh-intensitymechanicalandchemi-cal stimuli may cause activation and sensitization ofthe peripheral nerve endings and autonomic nerves,activatesecondorderneuronsincludingso-called“sleep-ing”receptors,causecentral sensitization,and lead tothe formation of new receptive fields, referred pain, along-lasting increase intheexcitabilityofnociceptors,andamoregeneralizedhyperalgesiabeyondtheinitialnociceptivearea.Anexpansionofareceptivefieldmeansthat a dorsal horn neuron receives information fromareasithasnotreceivedinformationfrompreviously218.Sensitizationofperipheralnerveendingscanalsocausepain through SP activating the neurokin-1 receptorsandglutamateactivating N-methyl-D-aspartaterecep-tors,whichopenspost-synapticchannelsthroughwhichCa2+ ionscanenter thedorsalhornandactivatemanyenzymesinvolvedinthesensitization85.

Severalhistologicalstudiesofferfurthersupportfortheintegratedtriggerpointhypothesis.In1976,Simonsand Stolov published the first biopsy study of MTrPsin a canine muscle and reported multiple contractionknots invarious individualmuscle fibers (Figure8)219.Theknotsfeaturedacombinationofseverelyshortenedsarcomeres in the center and lengthened sarcomeresoutsidetheimmediateMTrPregion219.

Reitingeretal220reportedpathologicalterationsofthemitochondriaaswellasincreasedwidthofA-bandsanddecreasedwidthofI-bandsinmusclesarcomeresofMTrPs in thegluteusmediusmuscle.Windischetal221determinedsimilaralterationsinapost-mortemhisto-logicalstudyofMTrPscompletedwithin24hoursoftimeofdeath.Menseetal222studiedtheeffectsofelectricallyinducedmusclecontractionsandacholinesteraseblockeronmuscleswithexperimentallyinducedcontractionknotsandfoundevidenceoflocalizedcontractions,tornfibers,andlongitudinalstripes.PongratzandSpath223,224dem-onstratedevidenceofacontractiondiskinaregionofanMTrPusinglightmicroscopy.NewMTrPhistopathologicalstudiesarecurrentlybeingconductedat theFriedrich

Fig.7: The integrated trigger point hypothesis.Ach- acetylcholine; AchE- acetylcholinesterase; AchR- acetylcholine receptor


Baur Institute in Munich, Germany. Gariphianova225described pathological changes with biopsy studies ofMTrPs,includingadecreaseinquantityofmitochondria,possibly indicating metabolic distress. Several olderhistologicalstudiesareoftenquoted,butitisnotcleartowhatextentthosefindingsarespecificforMTrPs.In1951,GlogowskyandWallraff226reporteddamagedfibrilstructures.Fassbender227observeddegenerativechangesof the I-bands, inaddition tocapillarydamage,a focalaccumulation of glycogen, and a disintegration of themyofibrillarnetwork.

Thereisgrowingevidencefortheintegratedtriggerpointhypothesiswithregardtothemotorandsensoryaspects of MTrPs, but many questions remain aboutthe autonomic aspects. Several studies have shownthat MTrPs are influenced by the autonomic nervoussystem. Exposing subjects with active MTrPs in theupper trapeziusmuscles to stressful tasksconsistentlyincreased the electrical activity in MTrPs in the uppertrapeziusmusclebutnotincontrolpointsinthesamemuscle,whileautogenicrelaxationwasable toreversetheeffects228-231.Theadministrationofthesympatheticblockingagentphentolaminesignificantlyreducedtheelectrical activity of an MTrP228,232,233. The interactionsbetweentheautonomicnervoussystemandMTrPsneedfurther investigation. Hubbard228 maintained that theautonomic features of MTrPs are evidence that MTrPsmay be dysfunctional muscle spindles. Gerwin et al184have suggested that the presence of alpha and betaadrenergicreceptorsattheendplateprovideapossiblemechanism for autonomic interaction. In a rodent,stimulationof thealphaandbetaadrenergicreceptorsstimulated the release of ACh in the phrenic nerve234.Inarecentstudy,Geetal61provided for the first timeexperimentalevidenceofsympatheticfacilitationofme-

chanicalsensitizationofMTrPs,whichtheyattributedtoachangeinthelocalchemicalmilieuattheMTrPsduetoincreasedvasoconstriction,anincreasedsympatheticreleaseofnoradrenaline,oran increased sensitivity tonoradrenaline.Anotherintriguingpossibilityisthatthecytokine interleukin-8 (IL-8) found in the immediatemilieuofactiveMTrPsmaycontributetotheautonomicfeaturesofMTrP.IL-8caninducemechanicalhyper-no-ciception,whichisinhibitedbybetaadrenergicreceptorantagonists235.Shahetal foundsignificantly increasedlevelsof IL-8 in the immediatemilieuof activeMTrPs(Shah,2006,personalcommunication).

ThefindingsofShahetal199markamajormilestoneintheunderstandingandacceptanceofMTrPsandsupportpartsof the integrated triggerpointhypothesis183.Thepossibleconsequencesofseveralofthechemicalspresentin the immediate milieu of active MTrPs have beenexploredbyGerwinetal184.Asstated,ShahetalfoundsignificantlyincreasedconcentrationsofH+,BK,CGRP,SP,TNF-α,IL-1β,serotonin,andnorepinephrineinactiveMTrPsonly.TherearemanyinteractionsbetweenthesechemicalsthatallcancontributetothepersistentnatureofMTrPsthroughvariousviciousfeedbackcycles236.Forexample,BKisknowntoactivateandsensitizemusclenociceptors,whichleadstoinflammatoryhyperalgesia,an activation of high-threshold nociceptors associatedwithC-fibers,andevenan increasedproductionofBKitself.Furthermore,BKstimulatesthereleaseofTNF-α,whichactivatestheproductionoftheinterleukinsIL-1β,IL-6, and IL-8. Especially IL-8 can cause hyperalgesiathat is independent from prostaglandin mechanisms.Viaapositive feedback loop, IL-1βcanalso inducetherelease of BK237. Release of BK, K+, H+, and cytokinesfrom injuredmuscle activates themusclenociceptors,therebycausingtendernessandpain184.

Calcitonin gene-related peptide can enhance thereleaseofAChfromthemotorendplateandsimultane-ouslydecreasetheeffectivenessofacetylcholinesterase(AChE)inthesynapticcleft,whichdecreasestheremovalof ACh238,239. Calcitonin gene-related peptide also up-regulates theACh-receptors (AChR)at themuscleandtherebycreatesmoredockingstationsforACh.MiniatureendplateactivitydependsonthestateoftheAChRandon the local concentrationofACh,which is the resultof ACh-release, reuptake, and breakdown by AChE. Insummary, increased concentrations of CGRP lead to areleaseofmoreACh,andincreasetheimpactofAChbyreducingAChEeffectivenessandincreasingAChRefficiency.Miniature endplate potential frequency is increased asaresultofgreaterACheffect.TheobservedloweredpHhasseveral implicationsaswell.Notonlydoesa lowerpHenhancethereleaseofCGRP,italsocontributestoafurtherdown-regulationofAChE.Themultiplechemicalsand lowered pH found in active MTrPs can contributetothechronicnatureofMTrPs,enhancethesegmentalspreadofnociceptive inputintothedorsalhornofthe

Fig.8: Longitudinal section of a contraction knot in a canine gracilis muscle (reproduced with permission from: Simons DG, Travell JG, Simons LS. Travell and Simons’ Myofascial Pain and Dysfunction: The Trigger Point Manual. Vol. 1. 2nd ed. Baltimore, MD: Williams & Wilkins, 1999)


spinalcord,activatemultiplereceptivefields,andtriggerreferredpain,allodynia,hypersensitivity,andperipheralandcentralsensitizationthatarecharacteristicofactivemyofascial MTrPs184. There is no other evidence-basedhypothesis that explains the phenomena of MTrPs inas much detail and clarity as the expanded integratedtriggerpointhypothesis(Figure9).

medical and psychological intervention64,82. CommonnutritionaldeficienciesorinsufficienciesinvolvevitaminB1, B6, B12, folic acid, vitamin C, vitamin D, iron,magnesium,andzinc,amongothers.The term“insuf-ficiency”isusedtoindicatelevelsinthelowerrangeofnormal, such as those associated with biochemical ormetabolicabnormalitiesorwithsubtleclinicalsignsandsymptoms.Nutritionalormetabolic insufficienciesarefrequently overlooked and not necessarily consideredclinicallyrelevantbyphysiciansunfamiliarwithMTrPsand chronic pain conditions. Yet any inadequacy thatinterfereswiththeenergysupplyofmuscleislikelytoaggravateMTrPs242.Themostcommondeficienciesandinsufficiencieswillbereviewedbriefly.

Vitamin B12 deficiencies are rather common andmayaffectasmanyas15%-20%of theelderlyandap-proximately 16% of persons with chronic MTrPs103,243.B12 deficiencies can result in cognitive dysfunction,degeneration of the spinal cord, and peripheral neu-ropathy, which is most likely linked to complaints ofdiffusemyalgia seen in somepatients.Serum levelsofvitaminB12ashighas350pg/mlmaybeassociatedwithametabolicdeficiencymanifestedbyelevatedserumorurinemethylmalonicacidorhomocysteineandmaybeclinically symptomatic244. However, there are patientswithnormallevelsofmethylmalonicacidandhomocys-teine,whodopresentwithmetabolic abnormalities ofB12 function242. Folic acid is closely linked to vitaminB12 and should be measured as well. While folic acidis able to correct the pernicious anaemia associatedwith vitamin B12 deficiency, it does not influence theneuromuscularaspects.

Iron deficiency in muscle occurs when ferritin isdepleted. Ferritin represents the tissue-bound non-es-sential iron stores in muscle, liver, and bone marrowthatsupplytheessentialironforoxygentransportandiron-dependentenzymes.Ironiscriticalforthegenera-tionofenergythroughthecytochromeoxidaseenzymesystemandalackofironmaybeafactorinthedevelop-mentandmaintenanceofMTrPs242.Interestingly,loweredlevels of cytochrome oxidase are common in patientswith myalgia140. Serum levels of 15-20 ng/ml indicateadepletionofferritin.Commonsymptomsarechronictiredness, coldness, extreme fatiguewithexercise, andmusclepain.Anaemiaiscommonatlevelsof10ng/mlorless.Althoughoptimallevelsofferritinareunknown,Gerwin242suggestedthatlevelsbelow50ng/mlmaybeclinicallysignificant.

Closeto90%ofpatientswithchronicmusculoskeletalpainmayhavevitaminDdeficiency245.VitaminDdeficien-ciesareidentifiedbymeasuring25-OHvitaminDlevels.Levelsabove20ng/mlareconsiderednormal,butGerwin242suggestedthatlevelsbelow34ng/mlmayrepresentinsuf-ficiencies.CorrectionofinsufficientlevelsofvitaminB12,vitaminD,andironlevelsmaytakemanymonths,duringwhichpatientsmaynotseemuchimprovement.

Fig. 9: The expanded MTrP hypothesis (reproduced with permission from: Gerwin RD, Dommerholt J, Shah J. An expansion of Simons’ integrated hypothesis of trigger point formation. Curr Pain Headache Rep 2004;8:468-475).Ach- acetylcholine; AchE- acetylcholinesterase; AchR- acetylcholine receptor; ATP- adenosine triphosphate; SP- substance P; CGRP- calcitonin gene-related peptide; MEPP- miniature endplate potential

perpetuating factorsThereareseveralprecipitatingorperpetuatingfactors

that need to be identified and, if present, adequatelymanaged to successfully treat persons with chronicmyalgia. Even though several common perpetuatingfactors are more or less outside the direct scope ofmanualphysical therapy, familiaritywith these factorsis critical especially considering the development ofincreasingly autonomous physical therapy practice.Simons, Travell, and Simons16 identified mechanical,nutritional,metabolic, andpsychological categories ofperpetuatingfactors.Mechanicalfactorsarefamiliartomanualtherapistsandincludethecommonlyobservedforwardheadposture,structuralleglengthinequalities,scoliosis,pelvictorsion,jointhypermobility,ergonomicstressors,poorbodymechanics,etc.16,102,116,240.

In recent review articles, Gerwin241,242 provided acomprehensiveupdatewithanemphasisonnon-struc-turalperpetuatingfactors.Managementofthesefactorsusuallyrequiresaninterdisciplinaryapproach,including


Even when active MTrPs have been identified in aparticularpatient,cliniciansmustalwaysconsiderthatMTrPs may be secondary to metabolic insufficienciesorothermedicaldiagnoses. It isquestionablewhetherphysical therapy and—as an integral part of physicaltherapy management—manual therapy interventioncan be successful when patients have nutritional ormetabolicinsufficienciesordeficiencies.Acloseworkingrelationshipwithphysicians familiarwith thisbodyofliterature is essential. Therapists should consider thepossibleinteractionsbetweenarthrogenicorneurogenicdysfunctionandMTrPs4,5,118,133,246,247.

Clinically, physical therapists should address allaspectsof thedysfunction.Therearemanyothercon-ditions that featuremuscle pain andMTrPs, includinghypothyroidism, systemic lupus erythematosis, Lymedisease,babesiosis,ehrlichiosis,candidaalbicansinfec-tions,myoadenylatedeaminasedeficiency,hypoglycaemia,and parasitic diseases such as fascioliasis, amoebiasis,andgiardia64,242.Therapistsshouldbefamiliarwiththesymptomsassociatedwiththesemedicaldiagnoses64.

PsychologicalstressmayactivateMTrPs.Electromyo-graphic activity in MTrPs has been shown to increasedramaticallyinresponsetomentalandemotionalstress,whereasadjacentnon-triggerpointmuscleEMGactivityremained normal229, 230. Relaxation techniques, such asautogenicrelaxation,candiminishtheelectricalactiv-ity231.Inaddition,manypatientswithpersistentMTrPsaredealingwithdepression,anxiety,anger,andfeelingsofhopelessness248. Pain-related fear and avoidance canlead to the development and maintenance of chronicpain249.Sleepdisturbancecanalsobeamajorfactorinthe perpetuation of musculoskeletal pain and must beaddressed.Sleepproblemsmayberelatedtopain,apnea,ortomooddisorderslikedepressionoranxiety.Manage-mentcanbebothpharmacologicandnon-pharmacologic.Pharmacologic treatment utilizes drugs that promotenormal sleep patterns and induce and maintain sleepthrough the night without causing daytime sedation.Non-pharmacologictreatmentemphasizessleephygiene,

such as using the bed only for sleep and sex, and notforreading,televisionviewing,andeating250.Therapistsmust be sensitive to the impact of psychological andemotional distress and refer patients to clinical socialworkersorpsychologistswhenappropriate.

The role of Manual TherapyAlthough the various management approaches are

beyondthescopeofthisarticle,manualtherapyisoneofthebasictreatmentoptionsandtheroleoforthope-dic manual physical therapists cannot be overempha-sized82,158. Myofascial trigger points are treated withmanualtechniques,sprayandstretch,dryneedling,orinjection therapy. Dry needling is within the scope ofphysical therapy practice in many countries includingCanada, Spain, Ireland, South Africa, Australia, theNetherlands, and Switzerland. In the United States,the physical therapy boards of eight states have ruledthat physical therapists can engage in the practiceof dry needling: New Hampshire, Maryland, Virginia,South Carolina, Georgia, Kentucky, New Mexico, andColorado80. A promising new development used in thediagnosis and treatment of MTrPs involves shockwavetherapy, but as of yet, there are no controlled studiessubstantiatingitsuse251,252.

summaryAlthough MTrPs are a common cause of pain and

dysfunction in persons with musculoskeletal injuriesanddiagnoses,theimportanceofMTrPsisnotobviousfrom reviewing the orthopedic manual therapy litera-ture.Currentscientificevidencestronglysupportsthatawarenessandaworkingknowledgeofmuscledysfunc-tion; in particular, MTrPs should be incorporated intomanual physical therapy practice consistent with theIFOMTguidelinesforclinicalpractice.Whiletherearestillmanyunansweredquestionswithregardtoexplain-ingtheetiologyofMTrPs,thisarticleprovidesmanualtherapistswithanup-to-dateevidence-informedreviewofthecurrentscientificknowledge.

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