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Year:1999|Volume:47|Issue:4|Page:2637

Dystonia:emergingconceptsinpathophysiology.
MMadhusudanan
DepartmentofNeurology,MedicalCollegeHospital,Kottayam,Kerala,686008,India.,India
CorrespondenceAddress:
MMadhusudanan
DepartmentofNeurology,MedicalCollegeHospital,Kottayam,Kerala,686008,India.
India

Abstract
Theessentialpathophysiologicalfeatureofdystoniaiscocontractionofantagonisticmuscles.Thismaybedueto
derangementofthespinalcordorcorticalmechanism.Inthecord,thereisdisruptionofthenormalreciprocalinhibition
ofantagonistsduringagonistcontraction.Thisdecreasedreciprocalinhibitionisduetoreducedpresynapticinhibitionof
muscleafferentinputtotheinhibitoryinterneuron.Thereducedpresynapticinhibitionmayinturnbeeitherdueto
defectivesuprasegmentalcontrolortochangesinthetonicafferentinputtotheinterneuronfromcutaneousand
muscleafferents.Alternatively,genesisofdystoniamayentirelybeacorticalmechanism.Overactivityofthepremotor
cortices,whichreceiveprojectionsfrombasalgangliaviaventralthalamus,couldresultindystoniabyabnormal
activationofcorticalmotorneurons.Thismayagainbeduetoadopaminergicdysfunctionofbasalganglia.

Howtocitethisarticle:
MadhusudananM.Dystonia:emergingconceptsinpathophysiology.NeurolIndia199947:2637

HowtocitethisURL:
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FullText

::Introduction

Dystoniaisdefinedasasyndromeofsustainedmusclecontractionsfrequentlycausingtwistingandrepetitive
movementsorabnormalpostures.Dystonicmovementsarealmostalwaysaggravatedduringvoluntarymovement
(actiondystonia).Idiopathicdystoniacommonlybeginswithaspecificactioni.e.actiondystonia.Theabnormal
movementsappearwithaspecificactionandarenotpresentatrest.Asthedystonicconditionprogresses,lessspecific
actionoftheaffectedlegmayactivatedystonia(e.g.whentappingthefloor).Withfurtherevolution,actioninother
partsofthebodycaninducedystonicmovementsofinvolvedleg(overflow).Withfurtherworsening,dystoniais
presentevenatrest.Eventuallythelimbgoesintosustainedposturing.Inadditiontothespecificbodypartshowing
progression,dystoniaoftenspreadstoinvolveotherpartsofthebody.Mostoftenthespreadistocontiguousbody

parts.Asageneralrule,theyoungerthepatientatonset,themorelikelyitisthatdystoniawillspread.Dystonic
movementstendtoincreasewithfatigue,stressandemotiontheytendtobesuppressedwithrelaxation,hypnosis
andsleep.Onecharacteristicanduniquefeatureisthattheycanbedecreasedbytactileorproprioceptivesensory
tricks.Thus,touchingtheinvolvedoradjacentbodypartcanoftenreducemusclecontraction.Thepathophysiologyof
dystoniaislargelyunknown.Theconceptthatbasalgangliadiseaseisexclusivelyresponsibleforgenesisofdystoniais
nolongertenable,sincelesionsinvariouspartsofthenervoussystemincludingthatofperipheralnervescancause
dystonia.

Inthisarticle,anattempthasbeenmadetopostulateareasonableexplanationforthepathophysiologyofdystonia
basedonvariousstudies.Eventhoughitiswellknownthatdystoniaresultsfromcocontractionofantagonistic
muscles,itwillbeinterestingtofindoutwhatcausesthiscocontraction,whyitisprecipitatedbycertaintaskspecific
actionandwhyitisrelievedbystimulationofcertaintriggerzones.

PATHOPHYSIOLOGYOFDYSTONIA

Pathophysiologically,theessentialfeatureisanabnormalcocontractionofagonistsandantagonists,[1]precipitatedby
certaintaskspecificactionandrelievedbycertainsensorytricks.Thereisalsocontractionofadjoiningmuscles
(overflow)particularlyduringvoluntarymovement.TheEMGinprimarytorsiondystoniashowscocontractionof
antagonisticmuscleswithprolongedburstsandoverflowtoextraneousmuscles.[2]Thisabnormalcocontraction,the
essentialfeatureofdystonia,couldtheoreticallyresultfromafaultatthespinalcordleveloratthecorticallevel.

Atthecordlevel,thereisabnormalityofthenormalreciprocalinhibitionbetweenagonistandantagonistsincasesof
dystonia.Studieshaveshownthatthesecondlongerphaseofreciprocalinhibitionisabsentorverymuchprolongedin
patientswithdystonia.[3]Thisdecreasedreciprocalinhibitionisduetothereducedpresynapticinhibitionofthemuscle
afferentinputtotheinhibitoryinterneuron.Thisreducedpresynapticinhibitioncouldinturnbetheoreticallydueto(a)
defectivedescendingcontrolor(b)changesinthetonicafferentinputtotheinterneuronfromcutaneousandmuscle
afferents.

Intramuscularinjectionofbotulinumtoxinindystonicpatientshasbeenfoundtoimprovetheinvoluntarymuscle
activityandimprovethereciprocalinhibitionbyincreasingthepresynapticinhibition.[4]Thisfindingsuggeststhatthe
toxinaltersthespinalcordsegmentalmotorsystem,byalteringthetonicsensoryinflowfromtheinjectedmuscles.
Thefactthatmuscleafferentshavearoleinproducingdystonicmovements,isalsoexemplifiedbytheworkofKayiet
al,[5]whostudiedthetonicvibrationreflexinwriter'scramp.Avibratorappliedonthehandinducedadystonicposture
andlocalinjectionoflidocaineintomusclesmarkedlydecreaseddystonicmovements.Grunewaldetalstudied
involvementofmusclespindlesinthepathophysiologyofdystonia,asmusclespindlesareinvolvedinthesensationof
positionandmovementofthebody.Theirexperimentsshowedabnormalperceptionofmotion,butnotposition,in
dystonicsubjects.[6]

Ontheotherhand,itistheoreticallypossiblethatcocontractionproducedbyalterationofreciprocalinhibitionmaybea
corticalmechanism,thisisbyalteringthedescendingcontrolonthepresynapticinhibition.Inzelbergetal[7]studied
thekinematicpropertiesofupperlimbtrajectoriesintorsiondystoniaandfoundthatmovementsindystonicpatients
wereslowandmorevariableandmovementtrajectorieshadaprolongeddecelerativecomponent,whichbecameeven

longerwithoutvisualfeedbackfromthelimb.Thesefindingssuggestthatdystonicpatientshavedefectsincentral
motormechanism.VanderKampetal[8]observedthatpeakamplitudeofmovementrelatedelectroencephalogram
potentialisreducedinpatientswitharmdystonia.Similarly,abnormalitiesincorticalpreparatoryprocessforvoluntary
musclerelaxationormotorinhibitionwasfoundinfocalhanddystoniabyYazawaetal,whostudiedtheBereitschafts
potentialsprecedingvoluntarymusclecontractionandrelaxation.[9]

Inhibitorycontrolofbasalgangliaoutputtothalamocorticalprojectionplaysanimportantroleinnormalcorticalactivity
inthecurrentmodelofthebasalgangliamotorcircuit.Excessorcollapseofthebasalgangliaoutputcanexplain
hypokineticandhyperkineticmovementdisordersofbasalgangliaorigin.Anabundanceofevidenceindicatesthat
parkinsonianakinesiaresultsfromhyperactivityofthebasalgangliaoutput.Reversalofakinesiabylesionsofthe
internaldivisionoftheglobuspallidus(GPi)oritsexcitatorysource,thesubthalamicnucleus,isconsistentwiththis
pathologicalschema.Ballismassociatedwithsubthalamiclesions,anddopainduceddyskinesiaareregardedas
hyperkineticdisordersresultingfromsuppressedsubthalamopallidalprojection.DecreasedfiringrateinGPiwasreported
inbothdisorders.However,pallidotomyhasrecentlybeenpostulatedtoabolishbothballismanddopainduced
dyskinesia.ApossiblemechanismfortheeffectofGPidestructioninthesehyperkineticdisordersmaybeblockadeof
thegenerationorconductionofphasicneuronalactivitiesdrivingchoreicmovements.Symptomatologically,dystonia
hasaspectsofbothhypokineticandhyperkineticdisorders.Overactivityofthepremotorcortices,whichreceive
projectionsfromthebasalgangliaviatheventralthalamus,wasfoundbothatrestandonmovementinidiopathic
dystonia.Thisabnormalcorticalactivitymayarisefromunderactivityofbasalgangliaoutput.Viteketal[10]did
microelectroderecordinginbasalgangliaof3patientswithgeneraliseddystoniaandfoundthatthemeandischarge
ratesofneuronsinbothsegmentsofthepallidumwereconsiderablylower.Inadditionthepatternofspontaneous
neuronalactivitywashighlyirregular,occurringasintermittentgroupeddischargesseparatedbyperiodsofpauses.This
findingofdecreasedneuronaldischargeratesofthepallidalneuronssuggeststhatthedystoniaisphysiologicallya
hyperkineticmovementdisorder.However,theameliorationofdystoniawithpallidotomysuggestsacomplex
pathomechanismofthepallidothalamicsystemindystonia.

Thetechniqueoftranscranialstimulationprovidedevidenceofchangesintheexcitabilityofmotorareas.Mavroudakis
etalshowedthatthepercentageincreaseintheareaunderneaththemuscleactionpotentialtraceevokedbybrain
stimulationisgreaterinpatientswithdystoniathaninnormalindividuals.Thissuggestsincreasedcorticalmotor
excitabilityindystonia.[11]Similarly,increasedexcitabilityofthecorticospinalmotorsystemwasfoundinwriter's
cramp,bynotinganincreaseinthecorticomotoroutputtotheaffectedhandduringrepetitivetranscranialmagnetic
stimulation.[12]

Inidiopathicdystonia,aninappropriateoveractivityofstriatofrontalprojectionandimpairedactivityofmotorexecutive
areashasbeenfound.UsingPETregionalbloodflowstudies,ithasbeenshownthatthereisoveractivityinthe
contralateralpremotorcortex,rostralsensorymotorarea(SMA),area8,anteriorcingulatearea32,ipsilateral
dorsolateralprefrontalcortexandbilaterallentiformnucleus.UnderactivityhasbeenfoundinthecaudalSMA,bilateral
sensorymotorcortex,posteriorcingulateandmesialparietalcortex.[13],[14]Thesefindingsmayexplainthe
coexistenceofdystonicposturesandbradykinesiainthesepatients.Theoveractivityofpremotorcortexandlentiform
nucleussuggestthathyperkineticmovementsobservedindystoniaisduetooveractivityofthepremotorcortex,which
inturnislinkedtolentiformnucleushyperfunction.Thelentiformnucleushyperfunctionleadstostructuraldisruption
ofbasalgangliainhibitorycontrolresultinginoveractivityofthepremotorcortex.Thusprimarydystoniaresultsfroma
functionaldisturbancesofbasalganglia,particularlyinthestriatalcontrolofglobuspallidus.Thiscausesaltered
thalamiccontrolofcorticalplanningandexecutiveareasandabnormalregulationofbrainstemandspinalcord
inhibitoryinterneuronalmechanism.[15]However,decreasedactivationofpremotorcortexwasseeninsomestudiesin
certaintaskspecificdystoniaslikewriter'scramp.IbanezetalstudiedregionalbloodflowinpatientsusingPETto
identifyregionsofmalfunction.Theynoteddecreasedactivationofpremotorcortexduringwritinganddecreased
correlationbetweenpremotorcorticalregionsandputamen.[16]Thissuggestsadysfunctionofpremotorcorticalnet

workinpatientswithwriter'scramp,possiblyarisingfrombasalganglia.Thusthedysfunctioniscompatiblewithlossof
inhibitionduringgenerationofmotorcommands,whichinturncouldberesponsibleforthedystonicmovements.

Reducedactivityofthecorticalinhibitorycircuitsinpatientswithdystoniahasbeenfoundbystudyingthecortical
excitabilitybymagneticstimulation.[17]Thisreducedfunctionofthecorticalinhibitorycircuitsmaybeonefactor
contributingtoexcessiveandinappropriatemusclecontraction,whichoccursduringtasksindystonicpatients.Ronaet
al[18]studiedthecorticalinhibitorymechanismswiththetechniqueofpairedtranscranialmagneticstimulationin
patientswithdifferenttypesofdystonias.Theyproposethatthealterationsobservedinpatientswithdystoniaarethe
resultofimpairedfeedbackfromthebasalgangliatomotorcorticalareas,withtheultimateeffectofaflatteningofthe
excitabilitycurveofthecorticalmotorneuronpoolduringvoluntarymusclecontraction.

Whataretheevidencesthatbasalgangliaisresponsiblefortheoveractivityofthepremotorcortexobservedin
dystonia?Innumerableclinicalcasestudieshaveshownthatthemostcommonsiteofaffectioninsymptomatic
dystoniaisbasalganglia,thattoomainlytheputamen.EvidencefromPETstudiessuggeststhatthelossofcortical
inhibitioninprimarytorsiondystonia(PTD)mightbecausedbyabnormalbasalgangliacircuitrywithanimbalance
betweenthedirectandindirectpathways.UsingnetworkanalysesofPET,Eidelbergetalfoundrelativebilateral
increasesinlateralfrontalandparacentralcortices,associatedwithrelativecovariatehypermetabolismofthe
contralaterallentiform,pons,andmidbrain.[19]Indystonia,incontrastwithParkinson'sdisease,lentiformand
thalamicmetabolismweredissociated,suggestingexcessactivityofthedirectputaminopallidalpathway.Magyar
Lehmannetal[20]confirmedthepathophysiologicroleoftheputaminopallidumpathwayintheirstudyofpatients
withtorticollis.Theyfoundincreasedbilaterallentiformglucosemetabolismthatdidnotcorrelatewithdiseaseseverity,
durationorsideofchinturning.

AnalternativeviewofbrainnetworksinprimarydystoniabasedonbothPETstudiesusingspiperonebindingand
animalmodelsusingMPTPhasbeenpresented.[21],[22]Itwasfoundthatpatientswithprimaryfocaldystoniahave
decreasedputaminalbindingofspiperone,aradioligandthatbindspredominantlytoD2likereceptors.MPTPtreated
baboonsdevelopedtransienthemidystoniapriortohemiparkinsonism.[22]Dystoniacorrespondedtemporallywith
decreasedstriataldopaminecontentandtransientdecreaseinD2likereceptornumber.Itwassuggestedthatdystonia
occursafterpreferentialdecreaseinD2mediatedinhibitionofstriatopallidalinhibitoryneuronsoftheindirectpathway.
Underthisscheme,medialpallidalinhibitoryoutputisincreasedtoyieldalossofsurroundinhibitionandoverflowofthe
motorcommand.Unlikeparkinsonism,however,thedirectpathwayisnotaffectedsothatselectionofthemotoraction
isnotimpeded.Thereisevidencetosuggestadisturbanceofdopaminergicfunctioninthepathophysiologyofearly
onsettorsiondystonia.Recentworkhasrevealedthatthecausativemutationinmostcasesisdeletionofaglutamate
residuefromthecarboxyterminalofTorsinA,a332aminoacidproteinencodedbytheDYT1gene.Thisproteinhas
similaritytothefamilyofheatshockproteinandClpproteases.However,itsfunctionandputativeroleinthenervous
systemremainsuncertain.Angoodetal[23]havemappedtheexpressionoftheDYT1geneinnormalhuman
postmortembrain.DYT1mRNAishighlyenrichedinthedopaminergicneuronsofsubstantianigraofparscompacta.
TheprominentexpressionoftheDYT1genewithintheparscompactaofsubstantianigrawhichprovidesdopaminergic
innervationtothebasalgangliaimplicatesadisturbanceofdopaminergicfunctioninthepathophysiologyofearlyonset
dystonia.Thisshowsadisturbanceofdopaminergicfunctioninthepathophysiologyofearlyonsettorsiondystonia.

Withtheaboveconceptsinmind,letustrytoanswertheimportantpathophysiogicalmechanismsindystonia.

1.Whythereisabnormalcocontraction?:Thisisduetothedownregulationofthereciprocalinhibitiondueto

changesinthepresynapticinhibition,whichagainmaybeeithercentrallymediatedorduetoaffectionoftheperipheral
afferentinput(eithercutaneousormuscle).

2.Whydystoniaistaskspecific?:Theabnormalcocontraction,themajordeterminantofdystonia,isnotthesole
abnormalityindystonia.Thereisanelementofhypokinesiainpatientswithdystoniaduetoimpairedactivityofthe
motorexecutiveareas.UnderactivityofcaudalSMA,bilateralsensorymotorcortex,posteriorcingulatecortexand
medialparietalcortexhasbeenshownbyPETstudies.Thustheremaybeamotorprogrammingdeficit,which
specificallyaffectscertainactionthanothers.Thismayexplainthetaskspecificityofdystonia.

3.Whydystoniaisrelievedbycertaintriggerpointstimulation?:Asalreadydiscussed,thecutaneousandmuscle
afferentshaveakeyroleinmodulatingthereciprocalinhibitionmechanismofthecord,inadditiontothedescending
motorcontrol.Botulinumtoxininjectionisfoundtoimprovethereciprocalinhibitionbyalteringtonicsensoryinflow
throughmuscleafferents.4Similarly,itishighlylikelythatcutaneousstimulationincertainpointsmaymodulatethe
presynapticinhibitionsoastoimprovethereciprocalinhibitionandtherebyalleviatingthecocontractionbetween
agonistsandantagonists.

4.Whatisthemechanismofoccupationaldystonia?:Itispossiblethatrepetitivestrainmayresultinalterationor
degradationofthesocalled`motorengrams'inthesensorymotorcorticalareaforaparticulartask.Thisissupported
byarecentstudydemonstratingthedevelopmentofdystoniaafterrepetitivestraininprimates.[24]Physiological
studiesinpatientswithsuchoccupationaldystoniashowdeficienciesinspinalreciprocalinhibitionandabnormalitiesof
centralsensoryprocessingandmotoroutputthatmayberelatedtoreducedcorticalinhibition.Recentstudiesin
primatessupportthenotionthatrepetitivemotionscaninduceplasticitychangesinsensorycortexleadingto
degradationoftopographicrepresentationofthehandandraisethepossibilitythatsensorytrainingmaybebeneficial.
[25]Subjectswithwriter'scrampwerefoundtohaveimpairedcapacitytointegratesensoryinformationinthemotor
programmingduringprecisiontasks,despitenormalsensibility.

Dystoniacanalsodevelopfollowingatemporarydisabilitytoalimb,e.g.inwristdrop.Ithasbeensuggestedthata
dystonicmovementdisordermaybecausedbypersistentmotorstrategiesadoptedtocompensateforatemporary
disability.[26]Itiswellknownthatlesionsotherthanthoseofbasalgangliacanalsocausedystonia.Maximumnumber
ofcasesofsecondarydystoniaareduetoaffectionofbasalganglia,especiallylentiformnucleus,caudatenucleusand
thalamus.[27],[28],[29]Itisnoteworthythatbasalganglialesioncanalsoproducefocaldystoniae.g.basalganglia
lesionscanproducecervicaldystonia,[28],[30],[31],[32]andblepharospasm.[33]Diffuseorfocaldystoniahasbeen
reportedduetolesionsofmesencephalon,[34]cerebellarlesion[35]pontinelesionduetocentralpontinemyelinolysis
withoutextrapontinemyelinolysis,[36],[37]medullarylesion[38]andspinalcordlesion.[39],[40]Focaldystoniawith
orwithoutassociatedcausalgiacanalsooccurduetoperipheralnervelesion.[41]Generalizeddystoniahasbeen
reportedinhomocystinuria,HIVinfection,aftermethanolingestionandasaremoteeffectofcarcinoma.

Tosumup,oneshouldenvisagedystoniaasaphenomenonwhichisnotspecifictoparticularsiteoflesion.Onemay
postulatetwotypesofdystoniaspathophysiologically,acceptingthatthemajordeterminantofdystoniaisabnormalco
contracionofmuscles:(1)acentralone,demonstratingtaskspecificityhavingvariationwithstress,fatigueetc.(2)a
peripheraloneproducingonlycocontractionresultinginabnormalpostureswithouttaskspecificityoroverflow.

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