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American College of Radiology (ACR). ACR Appropriateness Criteria—Primary bone tumors. 1995.
https://acsearch.acr.org/docs/69421/Narrative.AccessedJanuary11,2017.
NystromLM,ReimerNB,DeanCW,etal.Evaluationofimagingutilizationpriortoreferralofmusculoskeletaltumors:a
prospectivestudy.JBoneJointSurgAm.2015;97(1):10–15.
TurcotteRE.Giantcelltumorofbone.OrthopClinNorthAm.2006;37(1):35–51.
O’Keefe RJ, O’Donnell RJ, Temple HT, et al. Giant cell tumor of bone in the foot and ankle. Foot Ankle Int.
1995;16(10):617–623.
ZindrickMR,YoungMP,DaleyRJ,etal.Metastatic tumorsofthefoot:casereportandliteraturereview.Clin Orthop
RelatRes.1982;170:219–225.
OliveiraVC,vanderHeijdenL,vanderGeestIC,etal.Giantcelltumoursofthesmallbonesofthehandsandfeet:long-
termresultsof30patientsandasystematicliteraturereview.BoneJointJ.2013;95-B(6):838–845.
ZuoD,ZhengL,SunW,etal.Contemporaryadjuvantpolymethylmethacrylatecementationoptimallylimitsrecurrencein
primarygiantcelltumorofbonepatientscomparedtobonegrafting:asystematicreviewandmeta-analysis.WorldJSurg
Oncol.2013;11:156.
PorterDE,LonieL,FraserM,etal.Severityofdiseaseandriskofmalignantchangeinhereditarymultipleexostoses.A
genotype-phenotypestudy.JBoneJointSurgBr.2004;86(7):1041–1046.
QasemSA,DeYoungBR.Cartilage-formingtumors.SeminDiagnPathol.2014;31(1):10–20.
Driscoll M,Linton J, Sullivan E, et al. Correction andrecurrence of ankle valgus in skeletally immature patients with
multiplehereditaryexostoses.FootAnkleInt.2013;34(9):1267–1273.
Rupprecht M, Spiro AS, Schlickewei C, et al. Rebound of ankle valgus deformity in patients with hereditary multiple
exostosis.JPediatrOrthop.2015;35(1):94–99.
Gajewski DA, Burnette JB, Murphey MD, etal. Differentiatingclinicalandradiographic features ofenchondromaand
secondarychondrosarcomainthefoot.FootAnk leInt.2006;27(4):240–244.
RobertsEJ,MeierMJ,HildG,etal.Chondromyxoidfibromaofthecalcaneus:twocasereportsandliteraturereview.J
FootAnkleSurg.2013;52(5):643–649.
DaniilidisK,MartinelliN,GoshegerG,etal.PercutaneousCT-guidedradio-frequencyablationofosteoidosteomaofthe
footandankle.ArchOrthopTraumaSurg.2012;132(12):1707–1710.
TempleHT,MizelMS,MurpheyMD,etal.Osteoblastomaofthefootandankle.FootAnkleInt.1998;19(10):698–704.
Levy,DM,Gross,CE,Garras,DN. Treatmentofunicameralbonecystsofthe calcaneus: asystematic review.J Foot
AnkleSurg.2015;54(4):652–656.
ZhaoJ,DingN,HuangW, etal.Treatmentsforsimplebone cystsinthelongbones ofchildren.CochraneLibr. 2014.
http://www.cochrane.org/CD010847/MUSKINJ_treatments-for-simple-bone-cysts-in-the-long-bones-of-children.
SanerkinNG,MottMG,RoylanceJ.Anunusualintraosseouslesionwithfibroblastic,osteoclastic,osteoblastic,aneurysmal
andfibromyxoidelements.“Solid”variantofaneurysmalbonecyst.Cancer.1983;51(12):2278–2286.
GibbsCPJr,HefeleMC,PeabodyTD,etal.Aneurysmalbonecystoftheextremities.Factorsrelatedtolocalrecurrence
aftercurettagewithahigh-speedburr.JBoneJointSurgAm.1999;81(12):1671–1678.
Milgram JW. Intraosseous lipomas: radiologic and pathologic manifestations. Radiology. 1988;167(1).
http://pubs.rsna.org/doi/citedby/10.1148/radiology.167.1.3347718.
Toguchida J, Nakayama T. Molecular genetics of sarcomas: applications to diagnoses and therapy. Cancer Sci.
2009;100(9):1573–1580.
DesmanetE,Amrani M, FievezR,etal.LesAcrometastases. Aproposof2cases.Reviewoftheliterature.Ann Chir
MainMembSuper.1991;10(2):154–157.
AndreouD,RuppinS,FehlbergS. Survivalandprognostic factorsinchondrosarcoma: resultsin115patientswith long-
termfollow-up.ActaOrthop.2011;82(6):749–755.
AdkinsCD,KitaokaHB,SeideRK,etal.Ewing’ssarcomaofthefoot.ClinOrthopRelatRes.1997;343:173–182.
DemircayE,HornicekFJJr,MankinHJ,etal.Malignantlymphomaofbone:areviewof119patients.ClinOrthopRelat
Res.2013;471(8):2684–2690.
FletcherC,UnniK,MertensF.WHOClassification of Tumours. Pathologyand Geneticsof Tumours ofSoft Tissue
andBone.Lyon,France:IARCPress;2002.
HealeyJH,TurnbullAD,MiedemaB,etal.Acrometastases.Astudyoftwentyninepatientswithosseousinvolvementof
thehandsandfeet.JBoneJointSurgAm.1986;68:743–746.
LibsonE,BloomRA,HusbandJE,etal.Metastatictumorsofbonesofthehandandfoot:acomparativereviewandreport
of43additionalcases.Sk eletalRadiol.1987;16:387–392.
KaplanskyDB,KademianME,VancourtRB.Metastaticsquamouscell carcinomaresemblingcellulitisandosteomyelitis
ofthefifthtoe.JFootAnkleSurg.2006;45(3):182–184.
RamkumarU,MunshiNI,El-JabbourJN.Occultcarcinomaofthelungpresentingaspainin thehallux:a casereport.J
https://t.me/medicina_free
82.
83.
84.
FootAnkleSurg.2005;44(6):483–486.
SundbergSB,CarlsonWO,JohnsonKA.Metastaticlesionsofthefootandankle.FootAnkle.1982;3:167–169.
SimkinA,LeichterI,GiladiM,etal. Combinedeffectoffootarchstructureandanorthoticdevice on stress fractures.
FootAnkle.1989;10(1):25–29.
FottnerA,Baur-MelnykA,BirkenmaierC. Stressfractures presentingastumours: aretrospectiveanalysisof22cases.
IntOrthop.2009;33(2):489–492.
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CaseIllustration
PatientA
S.A.is a59-year-oldwomanwhohada nondisplacedright5thmetatarsalfractureinOctober1997.Shewas
treatedwithcaststabilizationfor8weeks.Shewasreferredtopainmanagementconsultation5monthsafterthe
injury.S.A.reportedthatshehadsufferedfromthrobbing,aching,andoccasionalshootingpainwhilewearingthe
cast. Symptoms escalated since cast removal. Movements and weather changes aggravated the pain. She
couldnottoleratewearingsockandwalkedwithacane.Herpainscoreonvisualanalogscorewas8/10.Bone
scanrevealeddiffuseincreasedvascularityanduptakeintherightlowerleg,ankle,andfoot(Fig.12-1).Theright
plantarskintemperaturewas29.7°Cversus28.7°Contheleft.Thepatient’shistory,symptoms,andsignswere
consistentwithearly-stagecomplexregionalpainsyndrome(CRPS).Diagnosticlumbarsympatheticnerveblock
(LSB) resulted in 2 to 3 days of significant pain relief. Thereafter, three more LSBs were performed with
concomitant physical therapy. Gabapentin (Neurontin) was also prescribed. Within 3 weeks, she reported
improvementof70%to80%.Shecouldwearshoesandwalkwithoutacane.
FIGURE12-1.Bonescanfromapatient4monthsafterright5thmetatarsalfracture.ClinicalCRPSdeveloped
within8weeksofinjury.
PatientB
D.C.isa30-year-oldmanwhosufferedarightfootandankleinjuryafterfallingthroughanimproperlycovered
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manhole.Therewas nofracture,buthe hadprogressivedebilitation and painintherightlowerextremity. He
described his pain as constant, sharp, and burning, from the tips ofthe toes to thegroin.Physical findings
included cold skinwith atrophic changes, limitedrange of motion, andinability to bear weight. He could not
toleratewearingashoeontheinjuredside.Hehadundergonetreatments,includingseveralkindsofmedication
(amitriptyline,tramadol,andgabapentin),physicaltherapy,andinvasivetreatmentswithLSBaswellas5daysof
localanestheticinfusionwithanepiduralcatheter.Hehadnolong-termrelief.About20monthsaftertheinjury,a
spinal cord stimulation trial (Fig. 12-2) produced immediate improvement. One week later, the permanent
stimulatorwasimplanted.D.C.continuestodowellat5-monthfollow-upwith70%lesspainmedication,andhe
couldtolerateaggressivephysicaltherapy.
FIGURE12-2.SpinalcordstimulatorinsertedatT10–T11witheightelectrodes.
INTRODUCTION
CRPS is difficult to diagnose and treat. So it has perplexed many physicians throughout
medicalhistory.Patientswithsuchaconditioninvariablycomplainedofseveredisablingpain,
yettheirhistoryofpresent illnessmayoften onlyamounttotrivialinjuries.Routineoreven
extensive investigations usually fail to reveal significant underlying causes. The baffled
physiciansunderstandablythinkthesepatientsexaggeratedtheirsymptomsandsufferings.Such
complainers were labeled neurotics and promptly referred to psychologists for “pain
management.” PatientswithCRPSaffecting their lowerextremities haveoftensuffered such
fates,andneverhadtheirconditiontreatedappropriately.
Recent animal and human studies have shed light on the pathophysiologyofthe CRPSrelatedgroupofconditions.Itisourintentiontodiscusssomeofthefootandankleconditions
thatwehaveseeninapainunitatanorthopediccenterthathavebeenassociatedwithCRPS
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1.
andtoreviewtheirtreatmentinlightofcurrentunderstanding.
BriefHistoricReview
In1864,Mitchellandcolleagues1firstdescribed,invictimsoftheAmericanCivilWarwho
sustainedbulletinjuriestotheirperipheralnerves,thesyndromeofseverelancinating,burning
pain in a limb that showed features of dystrophy. Later, Mitchell also named the condition
“causalgia,” from the Greek kausis (burning) and algos(pain).2 Since then, several similar
conditions,notnecessarilytheresultofpenetratinginjuriesbutsharingthecommonfeaturesof
burningpainwithdystrophy,havebeenrecognized.Inmanyofthem,evidenceofsympathetic
hyperactivity such as vasospasm, hyperhidrosis, and decreased skin temperature is also
present.Thesecausalgia-likeconditionsweregivendifferentnamessuchasposttraumaticpain
dysfunction syndrome, shoulder-hand syndrome, reflex neurovascular dystrophy,
neuroalgodystrophy,Sudeckatrophy,andothers.Theselabelsmakelong,interestinglists,but
they merely served to emphasize differences and reflect the disagreement regarding their
underlyingmechanisms.Therewasgeneralagreement,however,thatthesympatheticnervous
systemwassomehowinvolved,andexcessiveactivityinthisautonomicsystembroughtabout
the dystrophic changes. This led to the gradual adoption of the term “reflex sympathetic
dystrophy(RSD).”
As RSD implies, physicians are apt to believe that blocking the sympathetic pathway
wouldresultinresolutionoftheneuropathicsymptomsanddystrophy.Sympatheticblockade,
either with local anesthetics or with other means, became thepreferred treatment modality.
Disappointmentsoonsetin,however,whenitwasfoundthatmanyoftheRSDcasessimply
didnotrespondtosympatholysisand,therefore,couldnothavebeensympatheticallymediated.
By 1986, thetermsympatheticallymaintainedpain(SMP)asproposed byRoberts3 was
acceptedforthosecaseslabeledRSDthatrespondedtosympatheticblockade.TrueRSDwas
naturallyamemberofSMP.Othercasesthatmightnotshowmuchsympatheticoveractivitybut
yetrespondedtosympatheticblockadewerealsoincludedhere.Conversely,painconditions
thatshowedfeaturesofsympatheticoveractivityandevendystrophybutyetfailedtorespond
to sympathetic blocks were labeled sympathetic independent pain (SIP). It was later
recognizedthatSMPandSIPcouldrepresentthetwoendsofthespectrumforasingledisease
process.4 Despite improved nomenclature, much debate still continued as more underlying
mechanisms were proposed for the SMP–SIP syndromes. Further attempts to reduce the
confusionbroughtforthanotherrevisionintheterminology.AspecialConsensusWorkshopin
1993chosetheumbrellanamecomplexregionalpainsyndrome.4Toemphasizethedistinction
oftheoriginalcausalgia,CRPSwassubdividedintotwocategories:
CRPS-Icoversasyndromethat developsafteraninitiatingnoxiousevent.Spontaneous
pain or allodynia–hyperalgesia occurs. It is not limited to the territory of a single
peripheral nerve and is disproportionate to the inciting event. There is or has been
evidenceofedema,skinbloodflowabnormality,orabnormalsudomotoractivityinthe
regionofthepainsincetheincitingevent.Thisdiagnosisisexcludedbytheexistenceof
conditionsthatwouldotherwiseaccountforthedegreeofpainanddysfunction.RSDthus
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2.
fallsintothiscategory.
CRPS-IIis a syndrome similar toCRPS-Iexceptthatitdevelops afteraknownnerve
injury. Traditionally, these injuries involve largenerves, such as themedianor sciatic
nerve.
CLINICALFEATURES
HistoryofPresentIllness
CRPSmaypresentat thetime ofthe initial injuryorbedelayedfor weeks.CRPS-Ioccurs
withoutany known nerveinjury, whereas CRPS-IIhas anidentifiable nerve lesion.CRPS-I
maybeassociatedwithminor(e.g.,sprainsorbruises,skinirritation)ormajor(e.g.,fractures,
thermal or chemical burns, wound or joint infections, ischemic necrosis) injuries. In these
conditions,involvementofperipheralnervesiscommon.Itsassociationwithotherdiseasesin
whichdirectnervedamageisnotsoapparenthasalsobeenreported.Suchconditionsinclude
metastatic malignancy, Lyme borreliosis, diabetes, hyperthyroidism, hyperlipoproteinemia,
lumbarradiculopathyresultingfromlateraldiscfragment,previouslumbarlaminectomy,tarsal
tunnelsyndrome,andsoon.
Withouthistoryofsignificanttrauma,thepatientmayappeardisproportionatelydisabled,
frequentlywith startlingloss ofrangeofmotionifanextremityis affected.Ifthepatienthas
undergoneanoperation,aprotractedrecoveryperiodduringwhichthepatientpoorlytolerated
allrehabilitativeeffortsisacommonfeature.Storiessuchasthesewhenelicitedshouldraise
ahighindexofsuspicionandshouldpromptthesearchformorespecificCRPSfeatures.
SymptomsandSigns
The outstanding feature of CRPS pain is a spontaneous superficial burning sensation
superimposedon a continuousdeep,oftendescribed ascrushing, tearing,orthrobbing pain.
Exacerbation with movement is usual, but manypatients notice worse pain when resting at
night.Thereisoftenincreasedpainwithweatherchangesaswellasheatorcoldintolerance.
Patients usually shy away from bright sunshine and cold wind or even air conditioners.
Peculiar signsinthe affectedpartsincludeallodynia (painresultingfrom nonpainfulstimuli
such as light pressure), dysesthesia (unpleasant abnormal sensation such as stinging when
lightlyscratched),andhyperesthesia(increasedpainsensationtomildnoxiousstimulisuchas
apinprickor a heatlamp).Other findings maybemoreextensive spreadofpainthatis not
limitedtotheterritoryofasinglenerveordermatome.Vasomotor(Fig.12-3)andsudomotor
disturbancesmaybefoundinmore thanjusttheaffectedlimb.Inmore advancedorchronic
cases,structuralchangesoftheskinappendagesanddeepertissuesmaybepresent.
Variedsymptomsandsignsmaybegroupedaccordingtotheirseverity.In1953,Bonica
5
proposedacontinuumoftheRSDsyndromeusingstageItoIII.Later,Schwartzman6redefined
thestagesasacute,dystrophic,andatrophic,respectively.
Acute(StageI)
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Thisstagemayoccurimmediatelyorwithin daysoftheincitingevent.Itis characterizedby
spontaneouspainwithdysesthesiaandwarmskinwithlocalizededema.Thereisareluctance
totouchandmovetheaffectedbodypartasaresultoftendernessandmusclespasm.Increased
hairandnailgrowthmaybeseen.InearlystageI,thepainisusuallylimitedtothedistribution
oftheprincipalnervesinvolved.Theskinisusuallywarm,dry,andred,sometimesshowing
vasomotor instability including areas of erythema mixed with blanching. In late stage I,
however,thepainspreadsbeyondtheinvolveddermatomes,andtheskinbecomescyanoticor
mottledresemblinglivedoreticularis(Fig.12-4),cold,andclammy.Insomepatients,friction
fromclothingorlightairmovementontheskinmaycauseexcruciatingpain.Thereareusually
noradiographicbonechangesatthistime.
FIGURE12-3.PatientwithhistoryofCRPScausedbyblunttraumatotheleftfootshowingvasomotorinstability.
Noteerythematouspatchoverdorsumoffootthatisdistinctfromtheunaffectedrightfoot.
Dystrophic(StageII)
Dystrophicstageusuallysetsin3to6monthsfromtheonsetbutmayappearsoonerinrapidly
progressingcases.Thisstageisheraldedbyagradualincreaseintheareaofpain,extentofthe
edema,degreeofjointstiffness,extentofsofttissue,andmusclewasting.Theedemachanges
fromasofttoabrawny typewithglazedoverlyingskin.Moreadvancedchangesintheskin
appendagesare present. Thehair becomesscant, andthe nails become brittle,cracked,and
grooved. Disturbance of motor functions such as tremors or dystonia may be present.
Radiographicchangesappearinthisstage.
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FIGURE12-4.PatientwithCRPSresultingfromischemicnecrosis,whichrequiredtoeamputation.Patchy
erythemaandpallorproducedamottledappearance.
Atrophic(StageIII)
Thisstageischaracterizedbyadvancedtrophicchangesthataremostlyirreversible.Theskin
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issmooth,almostglossy.Itmaybepaleorcyanoticandfeelscoldasthetemperaturefurther
decreases. The hair becomes sparse and coarse. Subcutaneous tissue turns brawny as it
becomesatrophicwithmarkedlossoffat.Thedigitsarethinwithsevereatrophyofmuscles,
particularlytheinterossei.The interphalangeal andotherjointsoftheextremitybecomestiff
withdecreasedrangeofmotion.Theyeventuallyresultinankylosis.Painsymptomsmayhave
spread proximally or to other parts of the body. The affected parts are almost always
aggravated by passive motion or touching. Emotional disturbance and visual or auditory
stimulicanalsocausemarkedsuddenaggravation.
It should be notedthat in any individual case, there is usuallysome overlapping of the
features described in the different stages because the changes are seldom clear-cut. For
example, when the initial injury includes bone or joint trauma, osteoporotic changes may
appearwithinafewweeksinalimbthatotherwiseappearscompletelynormal.Furthermore,
vasomotorinstabilityandtrophicchanges, disparatethoughtheymayseem,arethoughttobe
manifestationsofaprogressivepathophysiologicprocess.
7
SYSTEMICSPREADOFCRPS
Long-standingCRPSpatientssufferpainthatspreadsbeyondtheareaofinitialinjury.Itoften
spreadsspontaneouslyto thecontralateral or ipsilateral limb.Diagonal patternof spread is
oftenassociatedwithnewtrauma.8Itwaspostulatedthatthe“pathologicimpulse”ofCRPSis
spread through the chain of sympathetic ganglia.9 CRPS patients often have constitutional
symptomssuchaslethargy,tiredness,orweakness.CRPSisaproinflammatorystatewherethe
body initiates nonspecific immune response following injury. The constitutional symptoms
experiencedbythesepatientsmaybeinpartbecauseofthisresponse.Studieshaveshownthat
thesepatientshaveincreasedheartrateanddecreasedheartratevariabilityduetogeneralized
autonomicimbalancerelatedtodisease duration,butnotpainintensity.10CRPSpatientscan
develop dystonia, affecting chest wall muscles leading to restrictive lung disease.11 These
patients can also feel chest discomfort that may be because of irritation of the
intercostobrachialnervethatinnervatespectoralandintercostalmuscles.Thischestdiscomfort
maybemistakenforcardiacpainorgallbladderdisease.12Thesepatientsoftensufferedfrom
boneandjointpain.ItisthoughtthatreleaseofsubstancePresultsinactivationofosteoclasts,
thusformingintracorticalexcavationduetobonedemineralizationandresorption.13Pathologic
fractures are common and often occur inthe 5th metatarsal bone. Inadditiontoskin color
changes,dermatologicmanifestationsincludedevelopmentofmorbilliformrash,punched-out
ulcer-likelesions,andrecurrentbullouslesions,tonameafew.
PATHOPHYSIOLOGY
DespiteadvancementinourunderstandingofCRPS,itspathophysiologyremainsuncertain.As
more knowledgeis gainedfrom the clinical observationsand experimental studies, there is
lessagreementinasinglecommonmechanism.Themanifestationofsomatosensoryandmotor
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disorders,autonomicdysfunction,andtissuestructuralchangesmakesitevenmoredifficultfor
cliniciansandscientiststoacceptasingleanimalmodelorhypothesisasthesolecauseforthis
disorder.
14
Whatisnowgenerallyacceptedisthatthereisexperimentalevidencethatsuggestspartial
injurytoamixedperipheralnervemayberesponsibleforatleastsomeofthefeaturesfoundin
CRPS.Undernormalconditions,sympatheticnervestimulationdoesnotexcitethenociceptors
(painreceptors) attheendingofanuninjured somaticnerve. Withindaysafterpartial nerve
injury, however, changes occur that render the nociceptors excitable by sympathetic
stimulation.Thenociceptors now alsorespondtointra-arteriallyinjectednorepinephrine.If
tissueinjury andinflammationhavealreadysensitizedthesenociceptors,theirresponsescan
befurtheraugmentedbysympatheticactivities.Someoftheproposedhypothesesthatlinkthis
local event of nociceptor sensitization to the generalized manifestation of sympathetic
hyperactivityareasfollows.
Inflammation
Tissueandnerve injury causesthe releaseofproinflammatorycytokines andneuropeptides,
such as interleukin6,tumornecrosis factoralpha,and substance P, inthe affectedarea. An
exaggerated localized inflammatory response is found inpatients withCRPS. Studies have
shown that CRPS patients have elevated levels of proinflammatory cytokines in their
cerebrospinal fluid compared to healthy controls as well as those with different types of
pain.
15
SympatheticDysfunction
Local tissue factors, includingsensitized nociceptors as well as neurotransmitter mediators,
mayactivatethesympatheticsystem.Inaviciouscycle,thenoxiousstimuliactivatesegmental
andsuprasegmentalsympatheticdischarges,producingvasoconstriction,ischemia,andfurther
nociceptoractivation.Theseresultinimpairedperfusion,whicheventuallyleadstodystrophic
changes.16 After tissue injury, abnormal connections between the sympathetic and somatic
nervous systems are established. The resulting cross-talk (called ephapses) between
sympatheticefferentandsomatosensoryafferentnervesexplainsthesympatheticcomponentof
thepainincausalgia.17In1983,Devor18presentedfindingshowingthatinflamedordamaged
peripheralnervetwigsformedabnormalsynapsesinthesamemannerasinjurednervetrunks.
Suchabnormalconnectionsallowedcross-talkbetweenthetwosystems,leadingtoincreased
signal input into the spinal cord, increased activity of the internuncial neuronal pool, and
furtherstimulationofthesympatheticefferentandsensoryafferents.
SpinalMechanism
TheneuronalturbulencehypothesisproposedbySunderland19in1976suggestedthatinjuryto
the postganglionic sympathetic ganglia and trans-synaptic degeneration in the spinal cord
wouldimpair thefunctionofspinalneurongroups.Thesegroupsofneuronscouldthenform
self-sustainingreverberatingcircuits.
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