a new rationale and treatment model for …...a physiological rationale for the cs treatment model...
TRANSCRIPT
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.