A New Rationale and Treatment Model for …...A physiological rationale for the CS treatment model is presented that incorporates concepts of central processing and the science of

ANewRationaleandTreatmentModelfor

NeuromuscularTenderPoints

BrianTuckeyPT,JayP.ShahMD,HannahTandonBA

©2017TuckeyContinuingEducationServicesLLC

Abstract

ThispaperpresentsanovelexpansionoftheosteopathictechniqueofStrain

andCounterstrain(SCS),originallydevelopedbyLawrenceJones,DO.WhileSCS

focusesonexaminingandtreatingthemusculoskeletalsystem,FascialCounterstrain

(CS),presentedhere,providesatreatmentandpathophysiologicalmodelthat

integratesallsystemsofthebodyintoJones’sconceptofneuromusculardysfunction.

InCS,TPs(includingtraditionalSCSTPs)areidentifiedandtreatedwithspecialized

fascialglidestargetedtolocalnociceptorsandmechanoreceptorsinsteadof

traditionalJonespositionsofcomfort.Additionally,thismodeloutlinesaprocessto

identifytreatmentsforpreviouslyundescribedneuromuscularTPs,twoofwhichare

describedinthepaper.Thesenewly-developedtreatmentshavebeenempirically

validatedthroughyearsofsuccessfulpatientoutcomesinavarietyofpatient

populations.

AphysiologicalrationalefortheCStreatmentmodelispresentedthat

incorporatesconceptsofcentralprocessingandthescienceoffascia.Neuronslocated

inthedeepfasciahavebothnociceptiveandmechanoreceptivepropertiesand

respondtolowthresholdpressurechanges.Repeatedperipheralnociceptiveinput

fromthefasciaintothecentralnervoussystemcancauseaprolongedorongoing

increaseinnociceptivepathwayexcitation,resultingincentralsensitization.This,

combinedwithsubsequentexcitationofperipheralnociceptors,caneffectivelycreate

system-specificTPs.CStreatmentsdecompresseslocalnociceptorsand

mechanoreceptors,mechanicallydeactivatingthem.Thisreducesperipheral

nociceptiveinputtothespinalcord,revertingcentralprocessingbacktoitsnormal,

non-excitedstate.

TheCScasestudypresentedisthatofcalcificshouldertendonitiswhichfailed

torespondadequatelytoarthroscopicsub-acromialdecompressionanda6-week

standardcourseofpost-operativerehabilitation.Thepatientwassubsequently

referredforatrialofCSinanattempttoavoidcalcificnoduleresectionandcomplete

rotatorcuffrepair.FollowingCStreatment,thepatientregainedfullstrength,full

rangeofmotion,andreportedsignificantpainrelief.Additionally,x-rayevidence

demonstrated100%reabsorptionofthecalcificnoduleinatimeframethatis92%

fasterthanaveragereabsorptiontimewithstandardtreatment.Thesepromisingcase

resultsandtheassociatedphysiologicalrationalesuggestthatCSprovidesaneffective

andtargetedmulti-systemtreatmentwhichmeritsfurtherstudy.

INTRODUCTION

FascialCounterstrainisamodern,expandedversionoftheosteopathictechnique

StrainandCounterstraininwhichallsystemsofthehumanbodyareassessedand

treated,notjustthemusculoskeletalsystem.Anewexplanationof

fascial/neuromusculartenderpointsispresentedthatutilizesthemodernconceptsof

centralprocessingandtheemergingscienceoffasciaasacontractilesensoryorgan.

Wesuggestthatthebodyprotectsalltissues,notjustmusculoskeletalstructures,via

nocifensivereflexesorchestratedbythefascialsystem.AFascialCounterstraincase

studyispresentedtodemonstratetheconceptofmulti-systemfascialmanipulation

anditspotentialimpactonamyriadofmusculoskeletalandnon-musculoskeletal

medicalconditions.

BACKGROUND

StrainandCounterstrain(SCS),alsoknownasPositionalRelease,isapassive

positionaltechniquedevelopedbyLawrenceJones,DO,aimedatrelieving

musculoskeletal(MS)andfascialpainthroughtheuseofindirect(non-painful,reflex-

based)manualmanipulation(D'Ambrogio&Roth1997).SCSisacommonformof

softtissuemanipulationpracticedbyosteopathicphysicians,physicaltherapists,and

othermanualmedicinepractitionersworldwide(Johnson&Kurtz2003;Saphyetal.

2016).

SCShasmultipleclinicalindicationsandhasbeenutilizedtotreatdisorders

involvingpain,edema,jointhypo-mobility,skeletalmuscletension,muscleweakness,

andfascialtension(Chaitow2007;D'Ambrogio&Roth1997;Wong2012).Initially,

tenderpoints(TPs)areidentifiedtodiagnoseneuromusculardysfunctionandare

monitoredoverthecourseoftreatmenttoassessclinicalprogress.Physically,TPs

weredescribedbyJonesas‘tense,tender,edematousmassesabout1cmindiameter’

andhavebeendocumentedinbothmuscularandfasciallocations(Chaitow2007;

D'Ambrogio&Roth1997;Jones1995).AfteradiagnosticTPisidentified,patients

arepassivelyplacedintospecifiedpositionsforupto90secondstoreleasetheTP

(Chaitow2007;D'Ambrogio&Roth1997;Jones1995;Wong2012).Intheclassic

SCSmodel,nodistinctionismadebetweenTPsandmyofascialtriggerpoints(Trps),

butadiscussionofhowtheyarerelatedwillbegivenlaterintheframeworkofthe

proposedCSmodel.

TheproposedphysiologicalmechanismsbehindSCSaretheoretical.

Historically,theproprioceptiveorKorrhypothesisofjointdysfunctionhasbeen

utilizedtoexplaintheeffectsofSCS(Wong2012).Inthistheory,aberrant

neuromuscularreflexescausedbydysfunctionalmusclespindlesleadtojointfixation

anddysfunction(Korr1975).Throughpassivepositioning,SCSisbelievedtoreset

thedysfunctionalproprioceptorstobaselinesensitivity,normalizingthestretchreflex

andrestoringpain-freefunctiontotheinvolvedjoint.

In1990,VanBuskirkquestionedthevalidityoftheproprioceptivemodel(Van

Buskirk1990).Hearguedthatmusclespindleactivityaloneisneithernecessarynor

typicallysufficienttoproduceisolatedskeletalmusclecontractionandthatother

tissueproprioceptorsexist,suchasnociceptorsthatcancauseasimilarclinical

presentation.Hearguedforanociceptivemodelthatcouldaccountforthefactthat

jointdysfunctionisknowntobecausedbynon-musculartissuesliketheviscera,

whichdonotcontainmusclespindles.In2005,theVanBuskirknociceptivemodel

wasupdatedtoincludenewresearchrelatedtotheexcitationofsegmentaldorsal

rootreflexesandthepotentialforpainmodulationfromdescendingCentralNervous

System(CNS)pathways(Howell&Willard2005).

ThescopeofSCStreatmenthasbeenexpandedoverthelast20yearsbythe

leadauthor,BrianTuckeyPT,OCS,(BT)adiscipleofJones.Oneofonlyfourphysical

therapiststobecertifiedtoteachSCSbyJones,BThasidentifiedover500previously

undocumentedneuromuscularTPs,asignificantnumberofwhichrequire

manipulationofnon-muscularstructuresinordertoalleviatetheclinicalsignsand

symptoms.WhilethesenewlyidentifiedTPsarelocatedinsurfacemuscleorfascial

tissues,manipulativeforcesaretypicallyappliedtounderlyinganatomicaltissues

includingthevisceralfascia(peritoneum),vascularfascia(tunicaadventitia),

ligamentsandallaspectsofthenervoussystem(epineurium).Thisnew,multi-system

formofSCSiscalledFascialCounterstrainorsimplyCounterstrain(CS)(Saphyetal.

2016;Tuckey2008,2011,2013,2014,2015a,b,c).CSTPsarebelievedtoimpactthe

functionofthespecificsystemstowhichtheyrelatethroughreflexiveconnectionsto

theCNS.Atheoreticalphysiologicalrationaleisofferedtoexplaintheeffectsofthis

newformofSCS,onethattakesintoconsiderationthemodernconceptsofcentral

sensitizationandtheexpandingroleoffasciaasasensoryorgan.

MATERIALSANDMETHODS

CStreatmentdiffersfromclassicSCStreatmentsdescribedbyJonesinthat

fascialglides,nottreatmentpositions,areutilizedtofacilitatearelease(Jones1995;

Tuckey2015c).ThefollowingsequencedetailsthestepsinvolvedinaCSTPrelease.

Thespecificphysiologicalchangesdescribedineachstepwillbediscussedlaterinthe

manuscript.

1) AdiagnosticTPisidentified.

2) Afascialglideorjointmovementisperformedthatunloadstheinvolved

structure.Thismanipulationisperformedtothespecifictissuethathasbeen

clinicallyidentifiedtoreleasetheTP.ThestructuremanipulatedmaybeMS,

visceral,neural,orvascularinorigin.

3) Thistissue-specificmanipulationdecompresseslocalnociceptorsand

mechanoreceptors,mechanicallydeactivatingthem.

4) Thetreatmentordecompressedpositionismaintainedfor15-45seconds.This

allowsanynoxioussubstancesinthesurroundingareatodissipate,alleviating

chemicalirritationoftheinvolvedperipheralnociceptors.

5) ThetechniqueisrepeatedtootherTPslocatedinthetargetedregion/limb/etc.

Thisreducesperipheralfascialnociceptiveinputtothespinalcord,reverting

centralprocessingbacktoitsnormal,non-excitedstate.

6) Fascialtonusisreducedandnocifensivereflexesarereturnedtonormal,

resolvingtissuetextureabnormalitiesandrestoringpain-freemobilitytothe

involvedstructures.

7) Sympatheticactivationisreducedascentralprocessingnormalizes,reducing

ischemiaandedemainthevascularbed.

8) Thepatientisre-assessedtoverifyresolutionoftheinvolvedTPsandtoassess

improvementsinpain,mobility,edema,function,etc.

Extensivemanipulativeexperienceandanatomicalknowledgeisrequiredto

identifyTPsnotpreviouslydescribedinSCS.InadditiontotrainingunderJones,the

author(BT)studiedmultipleformsofmanipulationovera26-yearperiodtogain

proficiencyinjointmobilitytestingandtheabilitytodifferentiate,usingpalpation,

betweendifferentsofttissuetypes(e.g.muscularvs.visceraltissues.)Thefollowing

sequencedetailsthegeneralempiricalmethodutilizedbyBTtoidentifyandname

newCSTPs.

(1) ThepatientisassessedandgivenCStreatmenttoallSCSTPspresent.

(2) Ifsymptomspersist,jointmotiontestingandtissuetextureabnormalitiesare

usedtoidentifyadditionalTPsnotpreviouslydescribedinSCS.

(3) IfaTPisidentified,regionaltissuesincludinglocalskeletalmuscle,ligaments,

neuro-vascularstructures,andtheunderlyingvisceraaremanipulatedina3-

dimensionalmanneruntilageneralvector(depth,directionandtissue

location)isidentifiedthatalleviatestheTP.Thismanipulationorglideisheld

for15-45secondsdependingontheseverityoftheTP.

(4) Followingasuccessfulrelease,thepatientisassessedtoidentify

improvementsorchangesinmobility,pain,digestion,sensation,strength,

balance,and/orotherobjective/subjectivefindings.

(5) AdditionalTPexaminationsandtreatmentsessionsareperformeduntilthe

patientreachesmaximumbenefitorthesymptomshavefullyresolved.The

reductioninperipheralnociceptionfollowingCStreatmentmayallowthe

associatedmaladaptiveCNSplasticitytonormalize,eveninsupraspinal

structureslikethethalamusorlimbicsystem.

TovalidateanewlyidentifiedTP,additionalpatientsareexaminedandtreated

untiltheexactvectorisverifiedthatconsistentlyresultsinalastingrelease.Thenew

TPisnamedbasedontheanatomicalstructurethatmaymatchtheTP’s3-

dimensionalvector.Wheneverpossible,thesuspectedanatomicalstructure(notjust

thesurfacediagnosticTP)ispalpatedfortissuetexturechangesbeforeandafter

treatmenttoverifytheassociation.Treatmentresponseandsymptomsareanalyzed

overtimetoconfirmthesuspectedanatomicalstructure.Forexample,anewly

identifiedTPisconfirmedtoberelatedtotheulnarnervewhentreatmentresolves

painandparesthesiasexperiencedinthe4thand5thdigits.

THEORETICALRATIONALEFOR‘FASCIAL’COUNTERSTRAIN

CSintegratesfasciaintotheSCSmodel.Therearetwotypesoffascia:

superficialanddeep.Superficialfascialiesbeneaththeskinandplaysarolein

thermoregulationandskinturgorandishighlyinnervated.Deepfascia,ontheother

hand,linesmusclegroupsandorgansandhaslongbeencalledthe‘organofform’

becauseofitsroleinofferingstructureandformtothehumanbody(Garfinetal.

1981).

Recentresearchhasdemonstratedthatdeepfasciaservesmorethana

structuralpurpose.Alltypesofdeepfascia,includingtunicaadventitia,peritoneum,

epineurium,andmyofascia(muscularfascia),havebeenshowntohaveextensive

proprioceptivepropertiesduetoTypeIIIandIVneurons(Feindeletal.1948;Mitchell

&Schmidt2011;Ruch1979;Schleip2003;Stacey1969;Stilwell1957a,b).These

neurons,rarelymentionedinphysiologicaltextbooks,arethepredominanttypesof

freenerveendingsindeepfascia.Thereceptorshavebothnociceptive(painsensing)

andmechanoreceptive(movementsensing)propertiesandrespondtoevenlow

thresholdpressurechangessuchaslighttouch(Mitchell&Schmidt2011).Thepain

experiencedthroughexcitationoffascialnociceptorsisvariableandcanrangefrom

dulltosharpandfromlocalizedtodiffuse(Geldard1974;Landau&Bishop1953).

Becausethedeepfasciaiseffectivelytheouterlayerofalltissues,ithasbeencalled

the“largestsensoryorgan”inthehumanbody(Schleip2003).Ingeneral,nociceptors

canbestimulatedbymechanical,chemical,orthermalmechanismsincludingpostural

strain,diseasestates,physicaltrauma,and/orinflammation(Mitchell&Schmidt

2011;Mountcastle1980;Schleip2003).Oncestimulated,peripheralnociceptorssend

signalstothespinalcord,activatingsecondaryneuronsthateventuallyascendinto

thepainperceivingregionsofthebrain(Fryer2016;Woolf2011).Thedorsalroot

ganglionneuronssubsequentlyreleaseinflammatorychemicalslikesubstanceP,

bradykinin,andcalcitoningene-relatedpeptide(CGRP)backintotheperipheral

tissuesviaantidromicnerveconduction.This‘dumping’effectofinflammatory

mediatorsbackintotheperipheryexacerbatestheexistingperipheralinflammatory

responsecausinghyperalgesia(abnormallyheightenedsensitivitytoanoxious

stimulus)(Willisetal.1998).

Nociceptoractivationmaystimulatetheautonomicnervoussystem.Themost

commoneffectofthisisanelevationinsympathetictoneorsympatheticnervous

systemactivation(SNA).Atthespinalcord,interneuronsandevensomeofthe

peripheralnociceptors'afferentsprojecttothepreganglionicneuronsoftheinter-

mediolateralcolumnproducingautonomiceffectsincludingvasopressor/vasodilator

effects,gastrointestinalstasis,andevenalterationsinimmunefunction(Benarroch

2006;Cortelli&Pierangeli2003;Foremanetal.1984;Irvinetal.1970;Johansson

1962;Mitchell&Schmidt2011;Purslow2010;Satoetal.1979).Othersomaticand/

orvisceralafferentsprojecttothemotorneuronsoftheventralhorn,drivingMS

protectivereflexescallednocifensivereflexes.SomeoftheseMSreflexesarelocal

whileothersaremulti-segmentalcontractionsthatthebodyutilizestominimize

noxioussensationswhichcanmanifestclinicallyaspain,limitedmobility,even

posturalasymmetry(Howell&Willard2005;Megirian1962).Inaddition,visceral

andsomaticafferentnervesareknowntoconvergeintothesameneuronsatboththe

spinalcord(dorsalhorn)andmidbrain(ventrolateralperiaqueductalgray)level.

ThesesharedvisceralandMSnocifensiveresponsesareknownasviscero-somaticor

somato-visceralreflexesandmustbeconsideredwhenevaluatingpatientswithorgan

and/orsomaticcomplaints(Cameronetal.2008;Foremanetal.1984).

SNAhasbeenshowntocauseongoingarterialvasoconstrictionandisknown

tobespinal-segmentspecificandthereforeorganspecific(Hijmeringetal.2002;

Malpas2010).Thesubsequentdisruptionofcirculationhasbeenassociatedwith

renalfailure,hypertension,andheartdisease(Malpas2010).Ongoingsympathetic

activationmayalsocauseadecreaseincirculationtomuscletissue,thelongterm

effectsofwhichwouldlogicallyleadtotrophicchangessuchasmusclefiberandor

tendondegeneration(Janig&Habler1995).

Furthermore,secondordernoci-responsiveneuronsinthespinalcordcanbe

stimulatedwhichascendviathespinothalamicandspinocervicothalamictractstothe

brainstemandthalamus(AbAziz&Ahmad2006).TheimpactontheCNScan

manifestassecondaryhyperalgesia(painlocatedoutsidetheprimaryareaofinjury)

andevenallodynia(paintoanon-noxiousstimulus)(Ruch1979;Woolf2011).This

conceptofcentralsensitization,whererepeatedperipheralnociceptiveinputintothe

CNScausesaprolongedorongoingincreaseinnociceptivepathwayexcitation,isa

well-establishedphenomenonwhichcansetupapositivefeedbackloopbetween

centralandperipheralnociceptors.Thisloopfostersthedevelopmentofchronicpain

conditionsincludingfibromyalgia,temporomandibulardysfunction,andvisceralpain

syndromes(Fryer2016;Woolf2011).

Additionalsupraspinalinfluencessuchasincreasedlimbicsystemactivitycan

alsooccurincasesofmyofascialpainsyndrome(MPS).Niddametal.demonstrated

increasedlimbicsystem(i.e.,anteriorinsula)activityinpatientswithuppertrapezius

MPSwhichcanaffectpainmodulationandpotentiallycausepsychologicalsymptoms

suchasfearandanxiety(Niddametal.2007).

Centralsensitizationandsubsequentexcitationofperipheralnociceptors

manifestsclinicallyaspressurehyperalgesia,whichlowerstissuepressurepain

thresholds,effectivelycreatingTPs(Woolf2011).Manyformsofosteopathic

diagnosishavebeenshowntohavepoorreliability;however,researchhas

demonstratedacceptableinter-examinerreliabilityusingtissuepalpationasa

diagnosticcriterionthussupportingtheuseofTPexaminationoverotherformsof

manualdiagnosessuchassegmentalmotiontesting(Seffingeretal.2004).

IntheCSapproach,TPsaretheprimaryfindingbywhichadiagnosisismade.

TheconceptofCSTPs(bydefinitiontense,tender,edematousmasses)accurately

describesthepresenceoftissueedemaaswellaslocalizedpressurehyperalgesia.

Thus,theclinicalsignsandsymptomsoftheCSTPcanbereasonablyaccountedforby

utilizingthemodernconceptsofcentrallystimulatednociceptors.Sincenociceptors

fromalltissuetypescanexciteinterneuronsatthespinalcordlevel,differentsystems

couldbeinjuredorinflamedandactastheprimarypainsourceorprimary

hyperalgesialocation.SecondaryhyperalgesiacanthereforeexistinsurfaceMS

locationsdespiteoriginatingfromacompletelydifferentinnervatedtissuesource

suchasavascularorvisceralstructure(Fryer2016;Meyeretal.2005).Oncecreated,

TPscanbemaintainedbycentralmechanismsincludingspinalplasticity(maladaptive

re-organizationofspinalcordneurons)orbycontinuedperipheralnociceptiveinput

aspatientscontinuetofunctioninthepresenceofactivatedorsymptomaticTPs

(Woolf&Salter2000).

Inadditiontothepresenceofnociceptorsandmechanoreceptors,researchhas

demonstratedthatfasciahasintrinsiccontractilepropertiesduethepresenceof

myofibroblasts(Purslow2010;Schleip2003).Schleipetal.(2005)measuredthe

forceofperimysialintermuscularfasciaandfoundittobesufficienttoimpact

musculoskeletalbehaviorand/orgammamotorneuronactivityaroundaninvolved

joint.Theabilityofdeepfasciatocontractmayhelpexplainthelastcharacteristicof

CStenderpoints:‘tissuetexturechange’orthefactthattenderpointsarepalpable,

eveninanatomicallyneutralpositions.Inthepast,paraspinaltissuetexturechanges

intheregionofpainhavebeenattributedtoreflexskeletalmusclecontraction,

however,morerecentstudieshavenotdemonstratedrestingEMGactivityatthe

locationoftissuechange,callingintoquestiontheideaofongoing,localizedalpha

motorneuronexcitation(Fryer2016).Aplausibleexplanationforalocalizedincrease

inpalpablemuscleand/orfascialtoneatrest,wouldbethatpractitionersareableto

perceivenotonlylocalizededemabutalsocontractedfasciarelatedtotheperipheral

orcentralexcitationoffascialnociceptors.Consideringthatperimysialfascia

contributestothepressureinsideamusclethroughitsstructural,physiological,and

metabolicproperties,itisconceivablethatperimysialfascialcontractioncouldcausea

clinicallyrecognizableincreaseinmuscletonus(Garfinetal.1981).

TheEffectofReducingofperipheralNociceptiveInputonCentralSensitization

In1992,Cohenetal.coinedtheterm‘refractorycervicobrachialpain’(RCBP)

afterobservingan‘epidemic’ofcasesinvolvingpatientswiththeclinicalfeaturesof

neuropathicpain(paininitiatedorcausedbyaprimarylesionordysfunctioninthe

nervoussystem)butinwhomnoradiculopathy,peripheralneuropathy,arthropathy,

ormyopathycouldbeidentified.Thesepatientspresentedwithallodynia,painon

jointmovement,cutaneoushypoaesthesia,andimpairedmotorfunction.Several

patientswhopresentedwithautonomicsymptoms,alsoreceivedsympathetic

(stellateganglion)blockswithoutconsistentresolutionofpainsymptoms,rulingout

sympatheticallymediatedpainastheprimarycause.Multiplesitesofanalgesic

and/orsympatheticblocks,however,werefoundtosignificantlyreducetheoverall

painpresentation.Thus,itwasconcludedthatRCBPisduetorepeatedperipheral

afferentnociceptiveinputfromanumberofpossibletissuesourcesincluding

capsular,muscular,and/orneuralstructuresresultingindorsalhornexcitation

(Cohenetal.1992).Thisconceptofreversingcentralsensitizationbyreducingthe

afferentbarrageofperipheralnociceptiveinputhasbeenexperimentallyand

theoreticallysupportedbyotherauthors.Graceyetal.(1992)performedlocal

anestheticblocksof‘painfulfoci’associatedwithprevioustrauma(essentially

blockingTPs)whichabolishedmechano-allodynia,coldallodynia,andspontaneous

paininallpatientsandrelievedthemotorsymptomsinonepatientwithtonic

contracturesofthetoes.Thesymptomsgraduallyreturnedastheanestheticwaned,

demonstratingthatperipheralnociceptioncandrivecentralsensitizationandis

apparentlyreversible.Insummary,Graceyconcluded:

‘Weproposeamodelofneuropathicpaininwhichongoingnociceptive

afferentinputfromaperipheralfocusdynamicallymaintainsalteredcentral

processingthataccountsforallodynia,spontaneouspain,andothersensoryand

motorabnormalities.Blockingtheperipheralinputcausesthecentralprocessingto

reverttonormal,abolishingthesymptomsforthedurationoftheblock.Themodel

accountsforsympatheticallymaintained(SMP)andsympatheticallyindependent

(SIP)pain.’(Gracelyetal.1992)

Althoughtheexactmechanismbywhichalteredcentralprocessingis

maintainedisstilldebated,Gracey’sfindingssuggestthattreatmentofperipheral

nociceptivesourcescanreversetheprocess.Hisresearchalsosupportstheconcept

thatcentralsensitizationcannotexistwithoutongoingnociceptiveinput.This

supportstheCSmulti-systemmodelthatutilizesthetreatmentofTPstoreducethe

numberofnociceptivesourcesintheperipheryandthusreducetheamountof

disabilityandpainexperiencedbypatientsduringactivitiesofdailyliving.

IntheliteraturethereisadistinctionmadebetweenfascialTPsandmyofascial

triggerpoints(Trps).TPsaredescribedasnon-specificsofttissuelocationsof

hyperalgesiathatdonotrespondtolocaltreatmentsandareoftenassociatedwith

widespreadpainsyndromeslikefibromyalgia(Schneider1995).Ontheotherhand,

Trpsarehard,palpable,tendernoduleslocatedinatautbandofskeletalmusclethat

havehistoricallyrespondedwelltolocaltreatments.Trpscanbeclassifiedaseither

activeorlatent.AnactiveTrpisassociatedwithspontaneouspain,andstrongdigital

pressureontheactiveTrpexacerbatesthepatient'sfamiliarpainexperience.Latent

Trps,ontheotherhand,arenotassociatedwithaspontaneouspaincomplaint;

however,pressureelicitspainlocallyatthesiteofthenodule.BothkindsofTrpscan

beassociatedwithmuscledysfunctionandweaknessandlimitedrangeofmotion.

ActiveTrpshaveelevatedlevelsofsubstancesknowntobeassociatedwithpain,

inflammation,sensitization,andintercellularsignalingascomparedtohealthy

skeletalmuscletissue(Shah&Gilliams2008).Thesebiochemicalsinclude

inflammatorymediators,neuropeptides,catecholamines,andcytokines.Thissupports

theconceptofactiveTrpsbeingareasofprimaryhyperalgesiacapableofinitiatingthe

processofcentralsensitization.

ItisimportanttonotethatinCS,thereisnodistinctionmadebetweenTPand

Trps.AllTrpsandTPscanbetreatedsuccessfullywithCSmanipulation.Whileinthe

literatureTrpsareoftendescribedsolelyintermsofmyofascia,CSconsidersa

potentialprotectiverelationshipofTrpswithunderlyingvisceral,vascular,andneural

tissuesrelatedtonocifensivereflexarcs.WhethertheyarepurelyMSorrelateto

anothersystemthroughthesereflexarcs,Trpsaremonitoredandreleasedinthe

samefashionasaTPfoundonabonylandmark.ThismeansinCS,Trpsare

essentiallyconsideredasubsetofTPs.ThereforeidentificationandnamingofaTrpin

CSfollowsthesameprotocolasthatforanyTP.

BecauseCSpractitionersdonotdistinguishTrpsfromthelargercategoryof

TPsforpurposesofassessmentandtreatment,fortheremainderofthisdiscussion,

‘TPs’willbeusedtodescribeallfocalareasoftissuetextureabnormalityincluding

thosethatcouldalsobedefinedasTrps.Forexample,Figure1illustratesaTP(which

inthiscase,fitsthedefinitionofaTrp)locatedintheproximalportionofthereflected

headoftherectusfemorismuscle.ThisTPempiricallyhasbeenfoundtonotrespond

tomanipulationofthequadricepshoweverdoesreleaseinresponsetoafascialglide

appliedtotheipsilateralileumandassociatedperitonealfascia.ThustheTPhasbeen

named‘ileum’insteadof‘rectusfemoris’(indicatingvisceral,notMSorigin).

(a) (b)

(b)

Figure1

RATIONALEFORMULTI-SYSTEMTPFORMATION

ThefollowingsequencedetailstheproposedmechanismofTPformationafter

recognizingfasciaasadynamic,multi-systemsensoryorganandincorporatingthe

conceptsofcentralsensitization.Thismodelisessentiallyanexpandedversionofthe

‘nociceptive’modelproposedbyVanBuskirkin1990:

1) Trauma,inflammation,posturalstrain,ordiseasestimulatesTypeIIIandType

IVfascialnociceptorsand/ormechanoreceptors.Theprimarynociceptive

tissuecanbemusculoskeletal,visceral,vascular,orneural.

2) Stimulatedperipheralnociceptorsactivateneuronsinthedorsalrootganglia

anddorsalhornofthespinalcord,causingexcitation.

3) Thesecentrallystimulatednociceptorsanti-dromicallyrelease,vianeurogenic

inflammation,chemicalslikeSubstancePandCGRPbackintotheperipheral

tissuescausinginflammation,leadingtoTPformation.

4) Insomeinstances,peripheralnociceptorscanexciteneuronsinthespinal

intermediolateralsystemcausingSNA.Thischronicincreasedsympathetic

activitywillcreatearterialand/orvenousvasoconstrictionpotentiallyleading

toorgandamage,impairedimmuneresponses,and/orMStrophicchanges.

5) Fascialcontractilitywillbestimulatedinthelocalarealeadingtoexaggerated

nocifensiveandgammamotorneuronreflexes,regardlessoftheunderlying

tissuesource.Thepatientwillpresentwithpain,limitedmobility,tissue

texturechanges,andimpairedfunction.

6) Thepatientwillsubsequentlyexperienceincreasednociceptiveinputasthey

mustfunctioninthepresenceofexaggeratednocifensivereflexesand

peripheralinflammation.

7) Secondorderspinalneuronswillberepeatedlystimulatedcarrying

nociceptiveimpulsestothebrainstem,limbicsystem,andthalamus.Thiscan

leadtoanexaggerationofnormalpainperceptionintheCNS,whichaddstothe

existinghyperalgesiaandperipheralnociceptiveinput.

8) PlasticityormaladaptivechangescanoccurintheCNSleadingtoallodynia,

furtherimpairingfunction.

9) Achronicstateofhyperalgesiaiscreated,withorwithoutsympatheticeffects,

inwhichallmovementthatgoesagainsttheestablishednocifensivereflexesis

limitedandpainful.IfSNAexists,arterial,venous,and/orlymphatic

vasoconstrictionwilloccur,limitingtheabilityofthesesystemstoremove

inflammatorymediatorsfromtheperipheryand/orleadingtotrophicchanges.

Thisaccountsforalargenumberofclinicalconditionsandsyndromeswhere

patientspresentwithMS,neural,visceral,and/orvascularsymptoms.

Thismulti-systemfascialmodelwouldprovideMSprotectionvianocifensive

reflexestoalltissues,notjustMStissues.Itseemsimprobablethatthebodywould

exclusivelyprotecttheMSsystem(viathegammamotorsystem)andnotcreatea

protectivemechanism,suchastheonedescribed,toprotectthemorevitalvisceral,

neuralandvascularstructures.

FASCIALCOUNTERSTRAINCASESTUDY

History:Alisha,a37-year-oldwhitefemale,presentedforanorthopedicconsultation

duetoasix-yearhistoryofleftshoulderpainanddisability.Thepainwasdescribed

asamaximumof10/10withactivitiesofdailylivingandreportedlydidnotrespond

tocortisoneinjection.

Diagnostictesting:TheoriginalMRI,performedthreemonthspriortothisvisit,

demonstratedalargecalcificnoduleintheSupraspinatustendonaswellasa

‘possible’SLAP(superiorlabraltear)lesion.Thecalcificnodulewasmeasuredat1to

1.5cmlong.AsubsequentMRIandX-rayperformedfollowingtheorthopedic

consultationverifiedtheexistenceofalargecalcificnodulewhichmadeup‘afairly

largepartoftheSupraspinatusattachment,especiallyanteriorly,’accordingtothe

attendingorthopedist.

Orthopedictreatment:Afterreviewingthepatient’sdiagnosticsandhistory,the

orthopedistrecommendedsub-acromialdecompressionwithdebridementofany

non-encapsulatedcalciumdeposits.

Surgicalintervention:Threeweekslater,asub-acromialdecompressionwith‘limited

calcificdebridement’wasperformed.Thecalcificnodulewasvisualizedduring

surgeryandwasnotremovedasitwas‘quitelarge’andexcisionwouldhaverequired

acompleterotatorcuffrepair.Followingshoulderdecompression,thepatientwas

referredforstandardpost-operativephysicaltherapyconsistingofmodalities,passive

stretching,andaprogramofstrengtheningexercises.

Resultsofdecompressionandstandardrehabilitation:Fivemonthsafterinitial

consultationandfourandahalfmonthsfollowingsub-acromialdecompressionand

standardrehabilitation,thepatientreturnedtotheorthopedistwithcontinued

complaintsofshoulderpainandfunctionalloss.Shehadbeendischargedfrom

physicaltherapyafterapproximately12visitshavingreachedmaximumbenefit.X-

raysperformedatthisvisitdemonstratednochangeinthecalcificnodulethathad

nowbeenpresentforatleasteightmonths(seeFigure2).

Three-monthsurgeryandrehabilitationfollow-up:Eightmonthsaftertheinitial

consultation,theorthopedistinformedthepatientthatshewouldrequireasecond,

moreinvasivesurgerytoexcisethecalcificnodule.Thissecondprocedure,duetothe

amountoftissuethatwouldneedtoberemovedduringtheexcision,wouldrequirea

completerepairoftherotatorcuff.

Atthattime,thepatientrequestedtobereferredtoBTforCStreatment,inan

attempttoavoidasecondsurgicalprocedure.

Figure2

Initialevaluation:Onemonthlater,theinitialphysicaltherapyevaluationandCS

treatmentwasperformed.DASH(disabilitiesofthearm,shoulder,andhand)index

demonstrateda56%disabilityscore.Thepainwasdescribedasincreasing,rateda

constant5/10intheshoulderandcervicothoracicspine.Thepatientreporteda

progressivedeteriorationinfunctionandwasunabletoreachoverheadorsleep

throughthenight.Shoulderflexionwaspainlimitedat140/180degreesand

abductionat100/180degrees.CSevaluationproceduresidentifiedmultiplesevere

vascular,neural,andMSTPsintheleft(involved)shoulderwhileonlyalimited

numberofmildTPswereidentifiedintheuninvolved(right)shoulder.Although

severalsystemsoffascialTPswereidentified,theTPsrelatedtothesympathetic

nervoussystemandSuprascapulararterywerefoundtobethemostsensitiveand

thereforediagnostic.IntheCSmodel,thisindicatedimpairmentofarterialperfusion

intheregionoftheleftshoulderandrotatorcuff(particularlytheSupraspinatus.)

CStreatment:InitialtreatmentconsistedofCStothepost-ganglionicsympathetics

fromC5toT3andtheSuprascapularartery(seeFigure3).Thesecondtreatment

(alsoexclusivelyCS)wastargetedprimarilytoaxillaryfasciaandneurovascular

bundletoimproveshouldermobilityandupperextremitybloodflow.Oversix

months,atotalof18sessionsofCSwereperformedtotheshoulder,TMJ,cervical

spine,andthoracicspineinordertoalleviatepainandrestorefunctionalrangeof

motionallinvolvedregions.

(a)

(b)

Figure3

CStreatmentresults:Afterthefirsttreatmentvisit,thepatientreportedthatshewas

abletosleepthroughthenightforthe‘firsttimesincethepainstarted,’sixyears

earlier.Bythe11thvisitshereporteda75%improvementinpainandwasableto

driveandreachoverheadwithoutpain.Hershoulderwasnolongersymptomatic,

andtreatmentfocusshiftedtoherTMJ,cervicalspine,andthoracolumbarspine(per

patientrequest).

EightmonthsafterinitiationofCStreatment,thepatienthadreturnedtofull

ADLsandwasnolongerbeingtreatedforhershouldercondition.Duringaroutine

follow-upvisitwithherorthopedist,shewasfoundtohavenormalstrength,normal

rangeofmotion,anegativeimpingementtest,andnear100%subjectivepain

(c)

reduction.X-raystakenthatdaydemonstratedfullandcompleteresolutionofthe

calcificnodule(seeFigures4and5).

Figure4

Figure5

CASESTUDYDISCUSSION

PriortoCStreatment,thispatienthadmorethansixyearsofshoulderpainand

functionaldisability.Hertreatmenthistoryincludedfourorthopedicconsultations,a

cortisoneinjection,asub-acromialdecompression,andsixweeksofstandardpost-

operativephysicaltherapywithoutresolutionofhercondition.Atthetimeofreferral,

thecalcificationwasclearlyvisibleonX-rayandwouldlikelyhavebeengradedinthe

moderatetosevererange(typeIorII)accordingtoGärtnerandHeyerduetothe

calcification’ssizeandwelldefinedborders(Gärtner&Heyer1995).

Theetiologyofcalcifictendonitisiscurrentlyunknown(Uhthoffetal.1976).

Researchhasdemonstratedthatcalcifictendonitis,whichoccurscommonlyin

youngerindividuals,isoftenaself-limitingcondition.Bosworthfoundtheaverage

rateofradiographicspontaneousresolutionofcalcificdepositstobe6.4%peryearor

15yearsforfullreabsorption(Bosworth1941).Thecalcificreabsorptionratecanbe

acceleratedwiththeadditionofnon-operativetreatmentaccordingtoWolkand

Wittenberg(Wolk&Wittenberg1997).Theyreportedasonographicresolutionrate

of82%within8.6yearswithconservativetreatment.Withregardstopain,research

demonstratesthatcalcifictendonitissymptoms(notcalcificationreabsorption)

requiresonaverage4.4yearstoresolvewithtreatment;however,itcantakeupto

13.5yearsinsomecases(Ogonetal.2009).

Inthiscasestudy,thepatienthadsignificantsymptomreduction(abletosleep

throughthenightforthefirsttimeinsixyears)afteronetreatmentwithCStargeted

tothesympatheticnervoussystemandvascularfascia.Fullresolutionofsymptoms

andcompleteradiographiccalcificreabsorptionwasachievedwithineightmonthsof

theonsetoftreatment,verifiedbyindependentorthopedicconsultationand

diagnostics(Figures4and5).Thisisasignificantlyshorterperiodoftimethanis

typicallyassociatedwithstandard,conservativetreatment(4.4yearsforsymptom

reliefand8.6yearsforcalcificreabsorption).Reabsorption,inthiscase,occurred

92%fasterthanaverage,possiblyduetothecontributionofCStreatment.Becauseno

radiographsweretakenbeforeeightmonthsafterinitiationoftreatment,itispossible

thatcalcificreabsorptionbeganevenearlier.Additionalresearchisneededto

determinetreatmentoutcomes,buttheresultsfromthiscasestudyarepromising.

WehypothesizethatthesecasestudyresultswereduetoareductioninSNA

followingtheapplicationofCStechnique.SuccessfulreleaseofmultiplefascialTPs

reducesnociceptiveinputtothespinalcord,leadingtoanormalizationofsympathetic

firingandreductionofcentralsensitization.Thisalleviatesvasoconstrictionand

improvesvascularperfusiontotherotatorcuff,thusrapidlyacceleratingthenatural

reabsorptionprocess.

CONCLUSION

FascialCounterstrainisanewlydevelopedclinicaltooldesignedtoreduce

nociceptiveinputfromallfascialsystemswiththeultimategoalofnormalizing

nocifensivereflexesandeliminatingcentralsensitization.Theproposedphysiological

rationalecanexplaintheexistenceoffascialtenderpointsandhowtheyrelateto

otherbodysystemsbyutilizingthemodernconceptsofcentralprocessingandthe

emergingscienceoffasciaasacontractilesensoryorgan.Wesuggestthatthebody

protectsalltissues,notjustmusculoskeletalstructures,vianocifensivereflexes

orchestratedbythefascialsystem.Whilefurtherresearchisneededtofullyvalidate

thetreatmentstrategydescribed,therationaleandcasestudypresentedsupportthe

useofFascialCounterstrainincasesofmusculoskeletalpainrelatedtosympathetic

nervoussystemactivation.Counterstrainhasthepotentialtoofferanewprimary

treatmentmethodfornumerousidiopathicmedicalconditionsthatareknowntoexist

invirtuallyeveryfieldofmedicine.

Acknowledgements

TheauthorBTisheartilythankfultohismentorsLawrenceJonesD.O.and

RandyKusunosePTwhofreelygavetheirtimeandknowledgesothathewasableto

gainexpertiseinStrainandCounterstrain.HewouldliketothanktheJonesInstitute

forprovidingaplatformandthelogisticalsupportnecessarytoreachaninternational

audiencewithFascialCounterstrain.Inaddition,BTwouldliketothankWilliamHall

Phdforhisresearchassistance,adviceandencouragementregardingpublicationof

thisarticle.Lastly,aspecialthankstoTimHodgesLMTforhissupport,friendshipand

relentlessdedicationtotheteachinganddevelopmentofFascialCounterstrain.

Citations

AbAzizCB,AhmadAH2006TheRoleoftheThalamusinModulatingPain.The

MalaysianJournalofMedicalSciences:MJMS13,11-18.

BenarrochEE2006Pain-autonomicinteractions.NeurologicalSciences27,s130-s133.

BosworthBM1941Calciumdepositsintheshoulderandsubacromialbursitis:a

surveyof12,122shoulders.JournaloftheAmericanMedicalAssociation116,2477-

2482.

CameronDM,BrennanTJ,GebhartGF2008Hindpawincisionintheratproduces

long-lastingcolonhypersensitivity.Thejournalofpain:officialjournalofthe

AmericanPainSociety9,246-253.

ChaitowL2007Positionalreleasetechniques.ChurchillLivingstone/Elsevier,

Edinburgh.

CohenML,ArroyoJF,ChampionGD,BrowneCD1992InSearchofthePathogenesisof

RefractoryCervicobrachialPainSyndrome.ADeconstructionoftheRSIPhenomenon.

MedicalJournalofAustralia156,432-436.

CortelliP,PierangeliG2003Chronicpain-autonomicinteractions.Neurological

Sciences:OfficialJournaloftheItalianNeurologicalSocietyandoftheItalianSocietyof

ClinicalNeurophysiology24Suppl2,S68-70.

D'AmbrogioKJ,RothGB1997Positionalreleasetherapy:assessment&treatmentof

musculoskeletaldysfunction.Mosby,St.Louis.

FeindelWH,WeddellG,SinclairDC1948Painsensibilityindeepsomaticstructures.

JournalofNeurology,Neurosurgery,&Psychiatry11,113-117.

ForemanRD,BlairRW,NealWeberR1984ViscerosomaticconvergenceontoT2–T4

spinoreticular,spinoreticular-spinothalamic,andspinothalamictractneuronsinthe

cat.ExperimentalNeurology85,597-619.

FryerG2016Somaticdysfunction:Anosteopathicconundrum.InternationalJournal

ofOsteopathicMedicine22,52-63.

GarfinSR,TiptonCM,MubarakSJ,WooSL,HargensAR,AkesonWH1981Roleof

fasciainmaintenanceofmuscletensionandpressure.JournalofAppliedPhysiology:

Respiratory,EnvironmentalandExercisePhysiology51,317-320.

GärtnerJ,HeyerA1995Calcifictendinitisoftheshoulder.DerOrthopade24,284-302.

GeldardFA1974TheHumanSenses,2ed.JohnWiley&Sons,Inc.,NewYork.

GracelyRH,LynchSA,BennettGJ1992Painfulneuropathy:alteredcentralprocessing

maintaineddynamicallybyperipheralinput.Pain51,175-194.

HijmeringML,StroesESG,OlijhoekJ,HuttenBA,BlankestijnPJ,RabelinkTJ2002

Sympatheticactivationmarkedlyreducesendothelium-dependent,flow-mediated

vasodilation.JournaloftheAmericanCollegeofCardiology39,683-688.

HowellJN,WillardF2005Nociception:NewUnderstandingsandTheirPossible

RelationtoSomaticDysfunctionandItsTreatment.OhioResearchandClinicalReview

15,1-4.

IrvinMK,KeithAB,ElliotLeeH,GeorgeWN1970Thepotentialdisruptiveinfluenceof

somaticinput,in:KugelmassIN(Ed.),ThePhysiologicalBasisofOsteopathicMedicine.

PostgraduateInstituteofOstopathicMedicineandSurgery,NewYork,pp.39-51,54.

JanigW,HablerHJ1995Visceral-autonomicintegration,in:GebbartGF(Ed.),Visceral

Pain:ProgressinPainResearchandManagement.IASPPress,Seattle.

JohanssonB1962Circulatoryresponsetostimulationofsomaticafferents.Acta

PhysiologicaScandanavia57,5-91.

JohnsonSM,KurtzME2003Osteopathicmanipulativetreatmenttechniquespreferred

bycontemporaryosteopathicphysicians.TheJournaloftheAmericanOsteopathic

Association103,219-224.

JonesLH1995Strain-Counterstrain.JonesStrain-CounterStrain,Boise.

KorrIM1975Proprioceptorsandsomaticdysfunction.TheJournaloftheAmerican

OsteopathicAssociation74,638-650.

LandauW,BishopGH1953PainfromDermal,Periosteal,andFascialEndingsand

fromInflamation:ElectrophysiologicalStudyEmployingDifferentialNerveBlocks.

A.M.A.ArchivesofNeurology&Psychiatry69,490-504.

MalpasSC2010Sympatheticnervoussystemoveractivityanditsroleinthe

developmentofcardiovasculardisease.PhysiologicalReviews90,513-557.

MegirianD1962BilateralFacilitatoryandInhibitorySkinAreasofSpinal

MotoneuronesofCat.JournalofNeurophysiology25,127-137.

MeyerRA,RingkampM,CampbellJN,RajaSN2005Neuralmechanismsof

hyperalgesiaaftertissueinjury.JohnsHopkinsAPLTechnicalDigest(AppliedPhysics

Laboratory)26,56-66.

MitchellJH,SchmidtRF2011CardiovascularReflexControlbyAfferentFibersfrom

SkeletalMuscleReceptors,in:TerjungR(Ed.),ComprehensivePhysiology.JohnWiley

&Sons,Inc.,Hoboken,NJ,USA.

MountcastleVB1980Medicalphysiology,14ed.C.V.MosbyCo,St.Louis.

NiddamDM,ChanR-C,LeeS-H,YehT-C,HsiehJ-C2007Centralmodulationofpain

evokedfrommyofascialtriggerpoint.TheClinicalJournalofPain23,440-448.

OgonP,SuedkampNP,JaegerM,IzadpanahK,KoestlerW,MaierD2009Prognostic

factorsinnonoperativetherapyforchronicsymptomaticcalcifictendinitisofthe

shoulder.Arthritis&Rheumatism60,2978-2984.

PurslowPP2010Musclefasciaandforcetransmission.JBodywMovTher14,411-

417.

RuchTC1979PathophysicologyofPain,Physiologyandbiophysics.Saunders,

Philadelphia,pp.272-324.

SaphyP,ÉtinneM,ThierryG,WosinskiJ,BellonL2016"StrainCounterstrain"du

nouveaudansl'approachduDr.LawrenceHJones.ProfessionKiné50,33-36.

SatoA,SatoY,SchmidtRF1979Theeffectsofsomaticafferentactivityontheheart

rate,in:BrooksCM,KoizumiK,SatoA(Eds.),IntegrativeFunctionsoftheAutonomic

NervousSystem.UniversityofTokyoPress/Elsevier.

SchleipR2003Fascialplasticity–anewneurobiologicalexplanation:Part1.JBodyw

MovTher7,11-19.

SchneiderMJ1995Tenderpoints/fibromyalgiavs.triggerpoints/myofascialpain

syndrome:aneedforclarityinterminologyanddifferentialdiagnosis.Journalof

ManipulativeandPhysiologicalTherapeutics18,398-406.

SeffingerMA,NajmWI,MishraSI,AdamsA,DickersonVM,MurphyLS,ReinschS2004

Reliabilityofspinalpalpationfordiagnosisofbackandneckpain:asystematicreview

oftheliterature.Spine29,E413-425.

ShahJP,GilliamsEA2008Uncoveringthebiochemicalmilieuofmyofascialtrigger

pointsusinginvivomicrodialysis:anapplicationofmusclepainconceptsto

myofascialpainsyndrome.JBodywMovTher12,371-384.

StaceyMJ1969Freenerveendingsinskeletalmuscleofthecat.JournalofAnatomy

105,231-254.

StilwellDL1957aTheinnervationoftendonsandaponeuroses.AmericanJournalof

Anatomy100,289-317.

StilwellDL1957bRegionalvariationsintheinnervationofdeepfasciaeand

aponeuroses.TheAnatomicalRecord127,635-653.

TuckeyB2008FascialCounterstrainfortheViscera.

TuckeyB2011FascialCounterstrainfortheLymphaticSystem.

TuckeyB2013FascialCounterstrainfortheArterialSystem.

TuckeyB2014JonesInstituteOriginatorsoftheStrainCounterstrainTechnique,

CounterstrainfortheNervousSystem:UpperBodyandCranium.

TuckeyB2015aFascialCounterstrainfortheMusculoskeletalSystemandBrain.

TuckeyB2015bFascialCounterstrainforthenervousSystemLowerQuadrant.

TuckeyB2015cIntroductiontoFascialCounterstrain.

UhthoffHK,SarkarK,MaynardJA1976Calcifyingtendinitis:anewconceptofits

pathogenesis.ClinicalOrthopaedicsandRelatedResearch,164-168.

VanBuskirkRL1990Nociceptivereflexesandthesomaticdysfunction:amodel.The

JournaloftheAmericanOsteopathicAssociation90,792-794,797-809.

WillisWD,SlukaKA,ReesH,WestlundKN1998Acontributionofdorsalrootreflexes

toperipheralinflammation,in:RudominP,RomoR,MendellLM(Eds.),Presynaptic

inhibitionandneuralcontrol.OxfordUniversityPress,NewYork,pp.407-423.

WolkT,WittenbergRH1997Calcifyingsubacromialsyndrome-clinicaland

ultrasoundoutcomeofnon-surgicaltherapy.ZOrthopIhreGrenzgeb135,451-457.

WongCK2012Straincounterstrain:currentconceptsandclinicalevidence.ManTher

17,2-8.

WoolfCJ2011Centralsensitization:implicationsforthediagnosisandtreatmentof

pain.Pain152,S2-15.

WoolfCJ,SalterMW2000Neuronalplasticity:increasingthegaininpain.Science

(NewYork,N.Y.)288,1765-1769.

FigureCaptions

Figure1.CSreleaseforIleum,visceraldysfunction(Tuckey2008).TPislocatedover

thereflectedheadoftheRectusFemorismuscle,justbelowtheupperrimofthe

acetabulum(superior,medial,anddeeptothegreatertrochanter)(a).Treatmentis

performedwiththepatientsupine,andfascialglideisappliedtotheileum,beneath

theumbilicus,inaposterior,lateral,andslightlyinferiordirectiontowardthe

acetabulum(b).

Figure2.Three-monthfollow-upX-raytakenaftersurgeryandstandard

rehabilitation.

Figure3.CSreleaseforC4-T5postganglionicsympatheticnerves(Tuckey2014,

2015c).TPsarelocatedovertheanterioraspectofthecervicaltransverseprocesses

fromC4-C6(a)andovertheinferioraspectoftheribtubercles2-5(b)(Notethatthe

TPsarenon-muscular).TopalpateTPlocationsapproachanteriortoposteriorforthe

C4-C5locationsandinferiortosuperiorfortheT2-T5locations.Treatmentis

performedwithpatientsupinepositioningtheshoulderintoflexionandadduction

withtheadditionofmildarmtractionasneededtoresolvetheTP(c).

Figure4.PostCStreatmentX-ray.

Figure5.PostCStreatment,physicianfollow-upnotes.