MEDI1012:TUTORGUIDE,WEEK2,NS2.

Updated: 22/04/2013

CaseTitle:Trapped.

Caseandtutorguidewrittenby:DrMichaelWalsh,DrShridarAtresh&DrMaryKelleher(2012)withthankstoDr
TerryTunnyandDrVaughanKippersforreview.

Case Summary: Ben is a 26 year old man who sustains a traumatic spinal cord injury. The case follows the clinical
presentationofanincompletetetraplegia.Thecaseisusedtointroducespinalcordanatomyandphysiology.Autonomic
physiology is explored in more detail as this is often a major issue in the care of people with spinal cord injury. Deep
venousthrombosis(DVT)andpressureareasareexploredascomplications.Thepsychosocialaspectsofspinalinjurywill
becoveredinasymposium.

Contextofthiscase:Thecaseisdesignedtointroducethestudentstotheconceptofspinalinjuryandtointroduce
spinalcordphysiology.Motorrootandsensoryrootanatomyisexploredwhilelearningaboutthelevelofinjury.The
Autonomicnervoussystemisexploredduringdiscussionoftheconstipationcausedbyspinalinjury.Pressuresoresand
DVTareexploredasconsequencesofimmobility.Psychosocialaspectsofspinalinjuryarediscussedintheseminar.

Keylearningissuesforthisweek:

KeyLearningIssues
Normalstructureanddevelopmentoftheaxial
skeletonandspinalcord

Functionalorganisationofthespinalcord

Dermatomes,myotomesandsclerotomes
Normalphysiologyofthespinalcord

Commonandseriousconditionsofspinalcord
Spinalcordinjury

TherapeuticInterventionsapplicableinspinal
cordinjury

FurtherExplanation
Embryology
Histology
GrossAnatomy
SurfaceAnatomy
Radiological

Sensoryreceptorsandpathways
Organisationofsensoryafferentfibresentering
spinalcord
Sensoryprocessinginthedorsalhorn
Ascendingsensorypathways(Spinothalamic
Tract&DorsalColumns)
Organisationofmotorsystems&locomotion
Uppermotorneurone
Descendingmotortracts(CorticospinalTract)
Musclespindleandlowermotorneurone
Spinalmotorneurones
Spinalcordreflexes

Autonomicnervoussystem
Parasympatheticdivison
Sympatheticdivision
Controlofbowel,bladderandsexualfunction
Pathophysiologicalmechanisms

OVERVIEWOF:
Epidemiology
Aetiologyandriskfactors
Clinicalfeatures
Diagnostictesting
Consequences
Principlesofmanagement
Roleofalliedhealthprofessionals

LearningObjectives
LO1

LO1

LO2,LO3,LO4,LO5,
LO6,LO7

LO3,LO5,LO6,LO7

Clinicalskillsassociatedwithspinalcordinjury

History&Examinationofpatientwithparalysis
Clinicalreasoningtogenerate,testandverify
diagnosesofpatientspresentingwith
paralysis/weakness
Approachtoprovidingasuccinctcasesummary
ofapatientpresentingwithparalysis/weakness

LO2,LO7

Assumedpreviousknowledge:StudentsshouldrevisethematerialthatwaspresentedduringtheYear1
introductoryweeks.Thelecturescovered

Anatomyofthecentralandperipheralnervoussystems
PeripheralNervousSystemincludingtheAutonomicandSomaticNervousSystems
Cellsofthenervoussystem
Classificationofnervefibres
Restingmembranepotentialandgenerationandpropagationofactionpotentials
Embryologicaldevelopmentofthenervoussystem
Pharmacologicalconceptsandneurotransmittersinvolvedinnervousfunctionandinthetreatmentof
dysfunctionalstates

ResourcesfortheWeek:

PleaselogontothestudentBlackboardsiteforthemostuptodatelistoflectures,recommendedreadings,topic
overviews,andotherresources.Pleasenotethatoccasionallychangesaremadetotheselistsduringthemodule,anditis
thereforeadvisedthatyouregularlycheckBlackboard(includingtheTutorCommunitysite)forupdatesand
announcementsinthisregard.

Informationfortutors:

SpinalCordInjury

Spinalcordinjury(SCI)isaninsulttothespinalcordresultinginachange,eithertemporaryorpermanent,initsnormal
motor,sensory,orautonomicfunction.Patientswithspinalcordinjuryusuallyhavepermanentandoftendevastating
neurologicdeficitsanddisability.

Thefollowingterminologyhasdevelopedaroundtheclassificationofspinalcordinjuries:

Tetraplegia(replacesthetermquadriplegia):Injurytothespinalcordinthecervicalregion,withassociatedlossofmuscle
strengthinall4extremities
Paraplegia:Injuryinthespinalcordinthethoracic,lumbar,orsacralsegments,includingthecaudaequinaandconus
medullaris.
ThepercentageofspinalcordinjuriesasclassifiedbytheAmericanSpinalInjuryAssociation(ASIA)isasfollows:
Incompletetetraplegia:29.5%
Completeparaplegia:27.9%
Incompleteparaplegia:21.3%
Completetetraplegia:18.5%
ThemostcommonneurologiclevelofinjuryisC5.Inparaplegia,T12isthemostcommonlevel.

Spinalcordinjurycanbesustainedthroughdifferentmechanisms,withthefollowing3commonabnormalitiesleadingto
tissuedamage:
Destructionfromdirecttrauma
Compressionbybonefragments,hematoma,ordiskmaterial
Ischemiafromdamageorimpingementonthespinalarteries
Oedemacouldensuesubsequenttoanyofthesetypesofdamage.

Spinalcordinjury(SCI),aswithacutestroke,isadynamicprocess.Inallacutecordsyndromes,thefullextentofinjurymay
notbeapparentinitially.Incompletecordlesionsmayevolveintomorecompletelesions.Morecommonly,theinjurylevel
rises1or2spinallevelsduringthehourstodaysaftertheinitialevent.

InAustralia,between20072008,therewere362newspinalcordinjuries.TheAustralianInstituteofHealthandWelfare
Report(20072008).
MostSCIsoccurintheyoung,between15to34years,althoughtherehasbeenarecentincreaseinSCIsinthoseover55
years.
MalesareapproximatelyfourtimesmorelikelythanfemalestosufferaSCI.Traumaaccountedfor79%ofthese
presentations.Transportrelated(46%)andfalls(28%)werethemaincontributors.
NontraumaticSCIisseenmorecommonlyinfemalesandolderpatientsandthespinalcorddamagetendstobe
incomplete.
Nontraumaticcausesofspinalcordinjuryincludethefollowing:
Vasculardisorders
Tumours
Infectiousconditions
Discdisease
Spinalcanalstenosis

Patientswithacompletespinalcordinjury(SCI)havealessthan5%chanceofrecovery.Ifcompleteparalysispersistsat72
hoursafterinjury,recoveryisessentiallyzero.Theprognosisismuchbetterfortheincompletecordsyndromes.
Ifsomesensoryfunctionispreserved,thechancethatthepatientwilleventuallybeablewalkisgreaterthan50%.
Ultimately,90%ofpatientswithspinalcordinjuryreturntotheirhomesandregainindependence.

Trigger1.1

PRESENTATION:

Benisa26yearoldmanwhowasdrivinghisutilityhomefromwork.Suddenlythecarinthenextlanetowingatrailer
ofpipesmergesintohislaneandlargepipespassthroughhiswindowandimpacthisneck.Benhearsacrackandfeels
anelectricshockthroughouthiswholebody.

Onarrivalattheemergencydepartmenthecomplainsofpinsandneedlesinhishandsandinabilitytomovehislegs.
Heishypotensiveandbradycardic,andgenerallyflaccidinhistriceps.Hisbreathingbecomeslaboured,hisoxygen
saturationsdropandheisintubated.

DiscussionPoints:

1.

Whatarethekeypointsobserved/describedinassessingthisman?

2.
3.
4.
5.
6.
7.
8.
9.
10.
11.

Youngmanwithtraumaticinjury
Hearsacrack.
Feelselectricshock.
Autonomicdysfunction.
Motordysfunction.
Sensorydysfunction

Whataretheimportantfeaturesofthispatientspresentation?Why?
Listhypothesesformechanismswhichwouldexplainthesesymptoms.
Whatisthestructureofthespinalcolumnandspinalcord?
Whatisthephysiologyofthespinalcord?
Whatistheautonomicphysiologyofthespinalcord?
Whatisthemostlikelyneurologicalinjury?
Atwhatlevelistheinjury?
Whataredermatomesandmyotomes?
Whyisheautonomicallyunstable?
Why,ifthediaphragmissuppliedbyC3,4,5,isherequiringrespiratorysupport?

NotesforTutors
Vertebralcolumn&spinalcord

Thereare7cervical,12thoracicand5lumbarvertebraethatarearticulatedand5fusedsacralvertebrae.Theyformthe
spinalcolumn.Thissurroundsthespinalcordwhichisahighlyorganizednetworkofafferentandefferentneuronesaswell
asinterneuronswhichmodulatethesignalsenteringandleavingthecord.
Themotorneuronsexittheventralaspectofthecordandhavetheircellbodieswithinthespinalcordwhilethedorsal
rootgangliawhichsitoutsidetheintervertebralforaminacomprisethecellbodiesoftheafferentsensoryneurons.

Thespinalcordisdividedintoacentralgreymatterregionshapedlikeabutterfly.Thegreymatterconsistsofthecell
bodiesoftheinterneuronsandmotorneurons.Thegreymatterissurroundedbyanumberoforganizedtractspassing
informationupanddownthecord.
ThespinalcorditselfendsintheconusmedullarisataboutL1/L2andcontinuesasacollectionofnerverootstermedthe
caudaequina.
Thesympatheticchainisachainofneuronswhichrunparavertebrallyfromthecervicaltosacralregion,thereare
sympatheticgangliawhichruninthischain.Thesympatheticchainreceivesafferentinputfromthecervical,thoracicand
lumbarnerveroots.

http://emedicine.medscape.com/article/1148570overview

Anatomy

http://img.medscape.com/pi/emed/ckb/clinical_procedures/113481511485701177.jpg


http://www.spinalinjury.net/html/_spinal_cord_101.html
Atwhatlevelisthisinjurylikelytohaveoccurred?

Theneurologiclevelofinjuryisthelowest(mostcaudal)levelwithnormalsensoryandmotorfunction.

Thedefinitionofthelevelofaspinalcordinjuryisdeterminedasthelastlevelwithastrengthof3outofapossible5.
Scoringforpower(strength)
0Completeparalysis(nomovement)
1Flickerofcontractionpossible
2Movementispossiblewhengravityexcluded
3Movementispossibleagainstgravitybutnotifanyfurtherresistanceisadded.
4Moderatemovementagainstresistance
5Normalpower
ThusapatientthathaswristextensorfunctionasthelastacceptablelevelisdefinedashavingaC6paraplegia.Thelevelis
determinedbythemyotomeinvolvediethespinalnerverootlevelmostresponsiblefortheactionofthatmuscle/muscle
group.

Thesensorylevelisdeterminedbythedermatomeinvolvedietheareaofskinsuppliedbyaspecificspinalnerveroot.
Sensoryscoringisforlighttouchandpinprick,asfollows:
0Absent
1Impairedorhyperesthesia
2Intact
Ascoreofzeroisgivenifthepatientcannotdifferentiatebetweenthepointofasharppinandthedulledge.

Forexample,apatientwithC5quadriplegiahas,bydefinition,abnormalmotorandsensoryfunctionfromC6down.

AmericanSpinalInjuryAssociation(ASIA)hasestablishedamethodforclassifyingspinalcordinjury(SCI)byneurologic
levelsasbelow.

AmericanSpinalInjuryAssociation(ASIA)hasestablishedamethodforclassifyingspinalcordinjury(SCI)byneurologic
levelsasbelow.

ASIAMUSCLESandSENSATION

ThefollowingkeymusclesaretestedinpatientswithSCI,andthecorrespondinglevelofinjuryisindicated:

C5Elbowflexors(biceps,brachialis)
C6Wristextensors(extensorcarpiradialislongusandbrevis)
C7Elbowextensors(triceps)
C8Fingerflexors(flexordigitorumprofundus)tothemiddlefinger
T1Smallfingerabductors(abductordigitiminimi)
L2Hipflexors(iliopsoas)
L3Kneeextensors(quadriceps)
L4Ankledorsiflexors(tibialisanterior)
L5Longtoeextensors(extensorshallucislongus)
S1Ankleplantarflexors(gastrocnemius,soleus)

Sensorytestingisperformedatthefollowinglevels:

C2Occipitalprotuberance
C3Supraclavicularfossa
C4Topoftheacromioclavicularjoint
C5Lateralsideofantecubitalfossa
C6Thumb
C7Middlefinger
C8Littlefinger
T1Medialsideofantecubitalfossa
T2Apexofaxilla
T3Thirdintercostalspace(IS)
T4FourthISatnippleline
T5FifthIS(midwaybetweenT4andT6)
T6SixthISatthelevelofthexiphisternum
T7SeventhIS(midwaybetweenT6andT8)

T8 EighthIS(midwaybetweenT6andT10)
T9NinthIS(midwaybetweenT8andT10)
T1010thISorumbilicus
T1111thIS(midwaybetweenT10andT12)
T12Midpointofinguinalligament
L1HalfthedistancebetweenT12andL2
L2Midanteriorthigh
L3Medialfemoralcondyle
L4Medialmalleolus
L5Dorsumofthefootatthirdmetatarsophalangeal
joint
S1Lateralheel
S2Poplitealfossainthemidline
S3Ischialtuberosity
S45Perianalarea(takenas1level)

AmericanSpinalInjuryAssociation(ASIA)methodforclassifyingspinalcordinjury(SCI)byneurologiclevel.
http://emedicine.medscape.com/article/793582overview

Whatisadermatomeandmyotome?

Amyotomeisthespinalnerverootlevelmostresponsiblefortheactionofthatmuscle/musclegroup.Adermatomeisthe
areaofskinsuppliedbyaspecificspinalnerveroot.

Whatisthemostlikelylevelofspinalcordinjury?
Benisunabletomovehislegsandisunabletoactivelyextendhiselbows(flaccidinbothofhistriceps).Thissuggestsmotor
injuryatC7.Healsohasparaesthesiaeofbothhands.ThehandsareinnervatedbythedermatomesC6C8inclusive.Ben
haslikelysustainedaspinalinjurywiththelastintactlevelC6.


Theskeletalinjurymaynotbeatthesamelevelastheneurologicalone.

Whyisheautonomicallyunstable(hypotensive&bradycardic)?

AutonomicinstabilitycanbecausedbybothSpinalandNeurogenicShock
(Othercausessuchashypovolaemiaandsepsisneedtobeexcluded)

Spinalshock
Spinalshockisatransitoryphenomenonwhichoccursjustaftertheinitialinjury.Inthiscasethereisareflexsuppressionof
spinalcordfunctionbelowtheleveloftheinjury.Flaccidparalysisofskeletalmuscle,bowelandbladderoccursaswellas
hypotension.Priapismmayalsooccur.Thesymptomsresolveafterreflexarcs(egmusclestretchreflex)inthespinebegin
tofunctionagainhourstodaysaftertheinjury.
Neurogenicshock
Neurogenicshockismanifestedbythetriadofhypotension,bradycardia,andhypothermia.Thisphenomenonisoftenseen
inanatomicallyhigherlesionsandisduetolossofsympatheticnervoustoneandconsequentunopposedvagalnerve
function.Thusvasodilationandbradycardia(twovagalaffects)areseen.
Neurogenicshockneedstobedifferentiatedfromspinalandhypovolemicshock.Hypovolemicshocktendstobeassociated
withareflextachycardia.

Why,ifthediaphragmissuppliedbyC3,4,5isherequiringrespiratorysupport?

TheIntercostalmuscleswhichareessentialaccessorymusclesforrespirationaredenervatedaswellastheabdominal
muscleswhichareusefulinexpiration.
Thepatientrequiresopportunityforrecoveryofaccessorymusclesandincreasingstrengthofdiaphragmaticmusculature.

OftenSpinalcordinjuryispatchyandapatientmayrecoverinanincompletefashion.ThusthetermCompleteno
recoverybelowthestatedlevelorIncompletepatchyrecoverybelowthestatedlevel.

Trigger1.2

INITIALMANAGEMENT&PROGRESS:

BenistransferredtotheintensivecarewardaftersurgerytostabilizeafractureoftheC6vertebra.Treatmentfor
hypotensionandrespiratorysupportisprovidedandslowlyhebecomesabletobreatheonhisown.

Overtheensuingdays,thereissomepatchyrecoveryofpowerandsensationinBensarmsandlegs.Smallflickersare
seeninsomemuscles.Themuscletoneinhislowerlimbsincreasesandhisreflexesinhislowerlimbsbecomebriskand
hedevelopsclonus.
Benbecomesquiteconstipated.

DiscussionPoints:

1.

WhatarethekeypointsinBensinitialprogress?

2.
3.
4.
5.
6.

Surgerytostabilisefracture
Intensivecaremanagement
Recoversabilitytobreatheindependently
Smallflickersofmuscleactivity
Somemotorandsensoryrecoveryinlimbs
Lowerlimbhypertonia
Lowerlimbhyperreflexiaandclonus
Constipation

Listhypothesesformechanismswhichwouldexplainthesesymptoms.
Whatistheautonomicphysiologyofthespinalcord?
Whyarethereflickers?
WhydoesBendevelopincreasedtoneandclonus?
Discussthemuscletendonreflexandexplainwhyitisincreased.

7.

Whatisthebasisoftheconstipation?Exploretheautonomicnervoussystemmorethoroughlyanddiscussother
examplesofdisordersofautonomicfunctionwhichmayoccurifdisrupted,consideralsobladderandsexualfunction.

NotesforTutors
Whyarethereflickers?
ItappearsBenslesionisincompletethusmusclefunctionrecoversslowlyandinapatchyfashion.

Whydoeshedevelopincreasedtoneandclonus?

Toneisdefinedasresistanceofmuscletopassivemovementatajoint.Tonecanbedecreased,normal,orincreased.
Clonusisasustainedrhythmicalcontractionofthemuscleswhenputundersuddenstretch.Itisduetohypertoniafroman
uppermotorneuronelesion.Itrepresentsanincreaseinreflexexcitabilityfromincreasedalphamotorneuroneactivity.
Increasedtone,increasedreflexesandclonusareallresultingfromlossofinhibitionofintrinsicspinalcordactivityby
highercentres.Thismaybeinapatchyfashiondependingonthepatternofrecovery.

Discussthemuscletendonreflexandexplainwhyitisincreased.
Themuscletendonreflexinamonosynapticspinalcordreflex.Theafferent(ingoing)signalcomesfromaspindlestretch
receptorinthemuscle.Asignalproducedbylengtheningofthestretchreceptor(bytapingitstendon)isfeddirectlyback
tothealphamotorneuroncontrollingthatmuscletoprovideanefferent(outgoing)signalwhichresultsinanantagonistic
contraction.Thesensitivityofthereflexisgovernedbysmallmusclefibresinthestretchreceptor,suppliedbyagamma
motorneuron.(Seediagrambelow)Itissubjecttoregulationviapathwaysfromthebrain.
Anincreasedjerkoccurswithanuppermotorneuronelesion.Adecreasedorabsentreflexoccurswithabreachinany
partofthereflexmotorarc.
Theincreaseintendonjerkreflexinspinalinjuryisacomplexprocess,thestudentsshouldunderstandthatasignificant
factoristhereductioninpresynapticinhibitionofthemotorneuronefromhighercentres.

10

SpinalReflexArc

11

What is the basis of the constipation? Explore the autonomic nervous system more thoroughly and discuss other
examplesofdisordersofautonomicfunctionwhichmayoccurifdisrupted.

Autonomicparasympatheticoutputtothelowercolonissuppliedbypelvicautonomicnerveswhichwillbelikely
interruptedbytheinjury.Thereisalsotheneedforresolutionofspinalshock(discussedabove).

TheAutonomicnervoussystemisaportionofthenervoussystemwhichessentiallygovernsautomaticsystemsincluding
heartrate,bloodpressure,bloodflowthroughskinandorgansaswellasdigestive,urinaryandsexualfunction.
Itisdividedintotheparasympatheticandsympatheticsystems.Broadlythetwosystemsareantagonisticbuttherearea
numberoffunctionswhichdonothaveanexactlyoppositeaction,forexamplethesympatheticsystemincreasesrateand
forceofcardiaccontractionwhiletheparasympatheticsystemonlyinnervatestheconductionsystemandhasnodirect
effectoncardiaccontractility.
Parasympatheticoutflowcomesfromcranialnervesandpelvicnerves(sacralsupply)whilesympatheticsupplycomesfrom
thoracicandlumbarroots.

http://www.austincc.edu/rfofi/NursingRvw/NursingPics/PNSefferentPics/sympatheticvsparasympatheticeffects.jpg

12

TheSympatheticsystemisinvolvedinthefright,flightorfightresponseandessentiallysecretescatecholamines(mostly
adrenalineandnoradrenaline)ontoitspostsynapticreceptors.TheParasympatheticsystemsecretesacetylcholineontoa
muscarinicpostsynapticreceptor.
Boththesympatheticandparasympatheticsystemshaveintermediategangliawhichareeitherparaspinal(sympathetic)or
inthetargetorgan(parasympathetic).
Everyefferentnervefromthespinalcordsecretesacetylcholineontoanicotinicreceptor.Thisistrueofskeletalmuscle,
parasympatheticgangliaandsympatheticgangliaaswellastheadrenalmedulla.

A=AcetylCholine,N=NicotinicReceptor,Na=Noradrenaline
M=MuscarinicReceptor,&areadrenergicreceptors

13

Autonomicdysreflexiaisamedicalemergencywhichoccursinspinalcordinjuredpatientsespeciallythosewithinjury
abovethemidthoraciccord.Inthissituationrelativelyminorstimuliegconstipation,afullbladderorevenapainful
ingrowntoenailcancauseamajorsympatheticoutflow.Thecauseisthoughttobeanaberrantreflexarccausedbylossof
theabilityofmessagesregardingtheabovestimulitobetransmittedpasttheinjuryduetolossofregulatorycontrolfrom
highercentres.Lifethreateninghypertensioncanresult.

NotesonBladder,Bowel&SexualFunctionanddysfunctionasaresultofspinalcordinjury

BladderFunction

Thenormalfunctionoftheurinarybladderistostoreandexpelurineinacoordinated,controlledfashion.
Thesephasesarecontrolledlargelybytheperipheralautonomicnervoussystem,withimportantmodulatinginformation
contributedbysensorynervesfromthebladderandurethra.FurthermodificationisprovidedbyhigherCNScentres,which
allowconsciouscontroloflowerurinarytractfunction.
Voluntarycontrolofdetrusoractivityisthoughttoariseinthefrontalcerebralcortex.Thisareaisincommunicationwith
thepontinemesencephalicreticularformation,whichservesasthebrainstemmicturitioncentre.
Aneuralloopinvolvingthebladder,sacralmicturitioncentre,pontinemicturitioncentre,andurethralsphincter
mechanismhasbeendescribed.Thispathwayallowsthecoordinationofurethralanddetrusorfunction.Coordinationof
urethralrelaxationwithdetrusorcontractionisdependentonthisneuralpathwaybeingintact.
Healthyfunctioningofthelowerurinarytractispartlydependentontheinterplayofsympathetic(ie,adrenergic)and
parasympathetic(ie,cholinergic)inputtothebladderandurethra.
Thesumeffectofsympatheticstimulationofthebladderandurethraisthepromotionofstorage.Parasympatheticor
cholinergicstimulationgenerallyismicturitionpromoting.

from
DRISLANE,F.etal.,2009.
rd
BlueprintsNeurology.3 ed.
Philadelphia:WoltersKluwer
Health.

14

Physiology
Normalbladderfunctionconsistsof2phasesfillingandemptying.Thenormalmicturitioncyclerequiresthattheurinary
bladderandtheurethralsphincterworktogetherasacoordinatedunittostoreandemptyurine.Duringurinarystorage,
thebladderactsasalowpressurereceptacle,whiletheurinarysphinctermaintainshighresistancetourinaryflowtokeep
thebladderoutletclosed.Duringurineelimination,thebladdercontractstoexpelurinewhiletheurinarysphincteropens
(lowresistance)toallowunobstructedurinaryflowandbladderemptying.
Fillingphase
Duringthefillingphase,thebladderaccumulatesincreasingvolumesofurinewhilethepressureinsidethebladderremains
low.Thepressurewithinthebladdermustbelowerthantheurethralpressureduringthefillingphase.Ifthebladder
pressureisgreaterthantheurethralpressure(resistance),urinewillleakout.
Thefillingoftheurinarybladderdependsontheintrinsicviscoelasticpropertiesofthebladderandtheinhibitionofthe
parasympatheticnerves.Thus,bladderfillingprimarilyisapassiveevent.
Sympatheticnervesalsofacilitateurinestorageinthefollowingways:
Sympatheticnervesinhibittheparasympatheticnervesfromtriggeringbladdercontractions.
Sympatheticnervesdirectlycauserelaxationandexpansionofthedetrusormuscle.
Sympatheticnervesclosethebladderneckbyconstrictingtheinternalurethralsphincter.Thissympatheticinputtothe
lowerurinarytractisconstantlyactiveduringbladderfilling.
Asthebladderfills,thepudendalnervebecomesexcited.Stimulationofthepudendalnerveresultsincontractionofthe
externalurethralsphincter.Contractionoftheexternalsphincter,coupledwiththatoftheinternalsphincter,maintains
urethralpressure(resistance)higherthannormalbladderpressure.Thecombinationofbothurinarysphinctersisknown
asthecontinencemechanism.
Thepressuregradientswithinthebladderandurethraplayanimportantfunctionalroleinnormalmicturition.Aslongas
theurethralpressureishigherthanthatofthebladder,patientswillremaincontinent.Iftheurethralpressureis
abnormallyloworiftheintravesicalpressureisabnormallyhigh,urinaryincontinencewillresult.
Emptyingphase
Thestoragephaseoftheurinarybladdercanbeswitchedtothevoidingphaseeitherinvoluntarily(reflexively)or
voluntarily.Involuntaryreflexvoidingoccursinaninfantwhenthevolumeofurineexceedsthevoidingthreshold.When
thebladderisfilledtocapacity,thestretchreceptorswithinthebladderwallsignalthesacralcord.Thesacralcord,inturn,
sendsamessagebacktothebladderindicatingthatitistimetoemptythebladder.
Atthispoint,thepudendalnervecausesrelaxationofthelevatoranisothatthepelvicfloormusclerelaxes.Thepudendal
nervealsosignalstheexternalsphinctertoopen.Thesympatheticnervessendamessagetotheinternalsphinctertorelax
andopen,resultinginalowerurethralresistance.
Whentheurethralsphinctersrelaxandopen,theparasympatheticnervestriggercontractionofthedetrusor.Whenthe
bladdercontracts,thepressuregeneratedbythebladderovercomestheurethralpressure,resultinginurinaryflow.These
coordinatedseriesofeventsallowunimpeded,automaticemptyingoftheurine.
Delayingvoidingorvoluntaryvoiding
Bladderfunctionisautomaticbutcompletelygovernedbythebrain,whichmakesthefinaldecisiononwhetherornotto
void.Thehealthyadultisawareofbladderfillingandcanwilfullyinitiateordelayvoiding.
Inahealthyadult,thePMC(pontinemicturitioncentre)functionsasanonoffswitchthatisactivatedbystretchreceptors
inthebladderwallandis,inturn,modulatedbyinhibitoryandexcitatoryneurologicinfluencesfromthebrain.Whenthe
bladderisfull,thestretchreceptorsareactivated.Theindividualperceivestheactivationofthestretchreceptorsasthe
bladderbeingfull,whichsignalsaneedtovoid.
Whenanindividualcannotfindabathroomnearby,thebrainbombardsthePMCwithamultitudeofinhibitorysignalsto
preventdetrusorcontractions.Atthesametime,anindividualmayactivelycontractthelevatormusclestokeepthe
externalsphincterclosedorinitiatedistractingtechniquestosuppressurination.
Thus,thevoidingprocessrequirescoordinationofboththeANSandsomaticnervoussystem,whichareinturncontrolled
bythePMClocatedinthebrainstem.

Pathophysiology
Ifaproblemoccurswithinthenervoussystem,theentirevoidingcycleisaffected.Anypartofthenervoussystemmaybe
affected,includingthebrain,pons,spinalcord,sacralcord,andperipheralnerves.Adysfunctionalvoidingconditionresults
indifferentsymptoms,rangingfromacuteurinaryretentiontoanoveractivebladderortoacombinationofboth.
Spinalcordinjury
Whenanindividualsustainsaspinalcordinjury,theinitialresponsefromthenervoussystemisspinalshock.Duringthis
spinalshockphase,theaffectedindividualexperiencesflaccidparalysisbelowthelevelofinjury,andthesomaticreflex
activityiseitherdepressedorabsent.
Theautonomicactivityisdepressed,andtheindividualexperiencesurinaryretention.Theinternalandexternalurethral
sphincteractivities,however,arenormal.
Thespinalshockphasetypicallylasts612weeks;itmaybeprolongedinsomecases.Duringthistime,theurinarybladder
mustbedrainedwithCICorindwellingurethralcatheter.

15

Afterdaystoweeks,thenervoussystemreactivates.Whenthenervoussystembecomesreactivated,itcauses
hyperstimulationoftheaffectedorgans.Diseasesorinjuriesofthespinalcordbetweentheponsandthesacralspinalcord
resultinspasticbladderoroveractivebladder.
Thesepeopleexperienceurgeincontinence(thebladderemptiestooquicklyandtoofrequentlymedicallytermed
detrusorhyperreflexiaoroveractivity).Inaddition,followingdisconnectionfromthepons,theexternalsphinctertendsto
contractwhenthedetrusoriscontracting.Thisinappropriatecontractionoftheexternalsphincterwithdetrusor
contraction(detrusorsphincterdyssynergia)canresultinurinaryretention,vesicoureteralrefluxandsubsequentrenal
damage.
Spinalcordinjuryproducesdetrusorhyperreflexia,lossofcomplianceanddetrusorsphincterdyssynergia.

SexualFunction

Althoughpsychicfactorsusuallyplayanimportantpartinthemalesexualactandcaninitiateorinhibitit,brainfunctionis
probablynotnecessaryforitsperformancebecauseappropriategenitalstimulationcancauseejaculationinsomeanimals
andoccasionallyinhumansaftertheirspinalcordshavebeencutabovethelumbarregion.Themalesexualactresults
frominherentreflexmechanismsintegratedinthesacralandlumbarspinalcord,andthesemechanismscanbeinitiatedby
eitherpsychicstimulationfromthebrainoractualsexualstimulationfromthesexorgans,butusuallyitisacombinationof
both.
Thesympatheticandparasympatheticdivisionsoftheautonomicnervoussystemcontrolthemalegenitalsystem.
Thetestes,epididymis,maleaccessoryglands,anderectiletissueofthepenisreceivedualinnervationfromthe
sympatheticandparasympatheticbranchesoftheautonomicnervoussystem(ANS).Thepenisalsoreceivesbothsomatic
efferent(i.e.,motor)andafferent(i.e.,sensory)innervationthroughthepudendalnerve(S2throughS4).
Erectionisprimarilyunderparasympatheticcontrol.
ThefirstandmostimportantpathwayforerectionistheparasympatheticdivisionoftheANS.Thesefibresderivefromthe
lumbarandsacralportionsofthespinalcordandtravelthroughthepelvicnerve,thepelvicplexus,andthecavernous
nervetothepenilecorporaandvasculature.Thispathwayisalmostentirelyparasympathetic.Theparasympathetic
activityresultsinvasodilatationofthepenilebloodvessels,thusincreasingbloodflowtothecavernoustissueand
engorgingtheorganwithblood.
Thesecondpathway,whichisthoughttobeentirelysympathetic,exitsthethoracolumbarspinalcord.Thepreganglionic
fibresthencoursethroughtheleastsplanchnicnerve,thesympatheticchain,andtheinferiormesentericganglion.The
postganglionicfibresreachthegenitaliathroughthehypogastricnerve,thepelvicplexus,andthecavernousnerves(see
earlier).Tonicsympatheticactivitycontributestopenileflaccidity.Duringerection,adecreaseinthissympathetictone
allowsrelaxationofthecorporaandthuscontributestotumescence.
Thethirdpathwayisthemotorbranchofthepudendalnerve.Ithasprimarilysomatic(i.e.,notautonomic)fibres,
originatesinthesacralspinalcord,andinnervatesthestriatedpenilemuscles.Humansareapparentlylessdependenton
theirstriatedpenilemuscleforachievingandmaintainingerection.However,thesemusclesareactiveduringejaculation
andcontributetotheforceofseminalexpulsion.
AfferentInnervationThepenisalsohasanafferentpathway.Thedorsalnerveofthepenisisthemainterminusofthe
sensorypudendalnerveandisthesoleidentifiablerootfortactilesensoryinformationfromthepenis.
Emissionisprimarilyundersympatheticcontrol.
Insummarythepudendalnervescarrybothmotorandsensoryfibresthatinnervatethepenisandclitoris.The
parasympatheticnervesarelocatedinthesacralcord(S2throughS4)andparticipateinerection.Thesympatheticnerves
arisefromcellsintheT11toT12levelsofthespinalcordthroughthehypogastricplexusandareimportantinejaculation.
LocaltissuemediatorssuchasnitricoxideandcGMPareprimarilyreleasedbyparasympathicticactivity,contributingto
sustainederection.

Pathophysiology
Sexualdrivepersistsfollowingspinalcordinjury(SCI),thoughsexualphysiologymaybealtered.Inmenwithuppermotor
neuronsyndromes,erectionsinresponsetolocalstimulation(reflexerections)arecommon,whileerectionsinresponseto
corticalstimuli,suchasthoughtsandsights(psychogenicerections),arelost.Reflexerections,whilecommon,maynot
persistlongenoughforsexualactivity.
Thosewithlowermotorneuronsyndromesdonotdemonstratereflexerections,butwhensympatheticoutflowfromthe
lowerthoracicandupperlumbarsegmentisspared,theymayhavepsychogenicerections.
Managementoferectiledysfunctioncanincludeexplorationofsexualexpressionnotinvolvingerection.Mostmenalsoare
interestedinoptionsforimprovingerectilefunction.Sildenafil(Viagra)hasproveneffectiveincasesofupperorlower
motorneuroninjury.Sildenafilistakenorally2060minutespriortothetimeofdesirederection.
AsubstantialproportionofwomenretainthecapacityfororgasmfollowingSCI,regardlessofseverityofinjury.Following
SCI,vaginalvasocongestioncanoccurinresponsetolocalstimulation.However,womenwithcompleteinjuriesaboveT6

16

donotdemonstratevaginalvasocongestioninresponsetopsychogenicstimulationalone;thisisbecauseoftheisolationof
thebrainfromthesympatheticoutflowtothegenitals.

Bowelfunction
Normaldefecationandanalcontinencearecomplexprocessesthatrequireacompetentanalsphinctercomplex,normal
anorectalsensation,adequaterectalcapacityandcompliance,andconsciouscontrol.
AnalSphincterComplex:thisneuromuscularcomplexconsistsoftheinternalandexternalanalsphinctermusclesandthe
puborectalismuscle.Theinternalanalsphincter(IAS)isthethickeneddistal3to4cmlongitudinalextensionofthecolon's
circularsmoothmusclelayer.Itisinnervatedbytheautonomicnervoussystemandcontributessubstantiallytothe
maintenanceoffaecalcontinenceatrest.Theexternalanalsphincter(EAS)consistsofstriatedmuscleandisprimarily
innervatedbysomaticmotorfibersthatcourseintheinferiorrectalbranchofthepudendalnerve.TheEASismainly
responsibleformaintainingfaecalcontinencewhencontinenceisthreatened.DuringdefecationtheEASrelaxestoallow
stoolpassage.Thepuborectalismuscleispartofthelevatoranimusclecomplexandisinnervatedfromitspelvicsurface
bydirectefferentsfromthethird,fourth,andfifthsacralnerveroots.Itsconstanttonecontributestotheanorectalangle,
whichaidsinpreventingrectalcontentsfromenteringtheanus.SimilartotheEAS,thismusclecanbecontracted
voluntarilyorinresponsetosuddenincreasesinabdominalpressure.
AnorectalSensation:Innervationtotherectumandanalcanalisderivedfromthesuperior,middle,andinferiorrectal
autonomicnerveplexusesthatcontainsympatheticandparasympatheticcomponentsandbyintrinsicnervespresentin
therectoanalwall.Inaddition,theinferiorrectalbranchofthepudendalnerveconveyssensoryinputfromtheloweranal
canalandtheskinaroundtheanus.Sensoryreceptorswithintheanalcanalandpelvicfloormusclescandetectthe
presenceofstoolintherectumaswellasthedegreeofdistension.Throughtheseneuralpathways,informationregarding
rectaldistensionandrectalcontentscanbetransmittedandprocessedandtheactionofthesphinctericmusculature
coordinated.
Therectoanalinhibitoryreflex(RAIR)referstothetransientrelaxationoftheIASandcontractionofEASinducedbyrectal
distensionwhenstoolfirstarrivesintherectum.Thisreflexismediatedbytheintrinsicnervesintheanorectalwall.
Followingintegrationoftheneuralinformation,defecationcanensueintheappropriatesocialsetting.Alternatively,if
required,defecationcangenerallybepostponed,astherectumcanaccommodateitscontentsandtheEASorpuborectalis
muscleorbothcanbevoluntarilycontracted.However,ifrectalsensationisimpaired,contentsmayentertheanalcanal
andmayleakbeforetheEAScancontract.
RectalAccommodationandCompliance:Therectumcanrelaxtoadmittheincreasedrectalvolumeinaprocessknownas
accommodation.Therectumisahighlycompliantreservoirthataidsstorageofstool.Asrectalvolumeincreases,anurge
todefaecateisperceived.Ifthisurgeisvoluntarilysuppressed,therectumrelaxestocontinuestoolaccommodation.
Pathophysiology
Neurogeniccolonicdysfunctionisaparticularlydistressingandlimitingimpairmentforasubstantialproportionofthose
withspinalcordinjury(SCI).Lowermotorneurondysfunction,aswithcaudaequinaandconusmedullarisinjury,causes
constipationwithslowcolonictransportandincontinenceduetoaflaccidsphinctermechanism.
Uppermotorneurondysfunctionalsocausesconstipationwithslowcolonictransitandstoolretentionbecauseofspasticity
ofthesphincterapparatus.However,withuppermotorneuroninjury,reflexesallowingdefaecationmayremainfunctional
andcanbeexploitedinestablishingabowelprogram.Thebowelprogramisaregimen,repeatedonadailyoreveryother
daybasis,thatcanincludediet,specifiedfluidintake,oralmedication,medicationperrectum,timing,andpositioning.The
goalsoftheprogramarecontinenceandconvenience.

http://emedicine.medscape.com/article/453539overview
http://emedicine.medscape.com/article/1265209overview#aw2aab6c17
http://emedicine.medscape.com/article/1265209overview#aw2aab6b8

17


Trigger1.3

NEUROLOGICALASSESSMENT

Onarrivalinthespinalinjuriesunit,fivedayslater,theRegistrarperformsaprogressneurologicalexamination.The
followingfindingsarenotedinthechart.
CranialnervesandfundoscopyNAD
Earlyatrophybothtricepswithfasciculationsandreducedtone
Power5/5elbowflexionandwristextensionbilaterally
TricepsPower1/5bilaterally
Reflexes
Tricepsjerk
Supinatorjerk

Bicepsjerk
Right
+
0
+

Left
+
0
+

Lowerlimbsnoatrophy,nofasciculations
Increasedtonealllowerlimbmusclegroups
Power2/5allgroups
Reflexes
Anklejerk
Plantar

Kneejerk
Right
+++
+++

Left
+++
+++

lighttouchandpinprickfromtoesproximallywithlowestnormallevelC6bilaterally.

DiscussionPoints

1. Whatarethekeypointsfromthistrigger?
Ongoingmanagementinspinalinjuryunit.
Progressneurologicalexamination.
2. Discusstheroleofthespinalinjuryunit.
3. Describethefindingsofthenervoussystemexamination.
4. DifferentiateUpperMotorNeuron(UMN)andLowerMotorNeuron(LMN)lesionsinthispatient.

NotesforTutors
Spinalinjuryunit

TheQueenslandSpinalInjuriesUnitisa40bedunitservicingallofQueenslandandNorthernNSW.Itissituatedatthe
PrincessAlexandraHospital,incloseproximitytoallotheracutemedicalservicesthatarerequiredtosuccessfullymanage
apersonwithSCI.
ItistheonlySpinalInjuriesUnitinQueensland.ItprovidesauniqueservicebeingtheonlySpinalInjuriesUnitinAustralia
thatprovidesacutecare,primaryrehabilitation,transitionalrehabilitation,outpatientservicesandoutreachservices
(education&trainingforpeoplewithSCI,families,carers)andcommunityservicesfromtheonefacility.

TheSpinalInjuriesUnitprovidesmultidisciplinaryexpertisein:
PhysicalRehabilitation
BladderandBowelCare
SexualandFertilityIssues
PressureSoreManagement
PsychologicalIssues
FunctionalSkillsTraining

18

HomeAssessment
CareofVentilatorDependantClients
TendonTransferSurgery
SeatingandPosturalIssues
SpinaBifidaClinic
PainManagement
ComplicationsofSCI.

Rehabilitationservicesareprovidedbyanexperiencedmultidisciplinaryprofessionalteam.(Doctors,Spinalcordinjury
andRehabilitationspecialists,Nurses,OccupationalTherapists,Physiotherapists,SocialWorkers,
Pshychologist/Neuropsychologist,SpeechTherapists,ActivitiesNurse,Dietician,OrthoticsandProstheticService,
SupportStaff,OtherMedicalandSurgicalSpecialtyStaff)

Theprimarygoalsofrehabilitationarepreventionofsecondarycomplications,maximizationofphysicalfunctioning,and
reintegrationintothecommunity.

RehabilitationfollowingSCIismosteffectivelyundertakenwithamultidisciplinary,teambasedapproach,asfollows:

Physiotherapiststypicallyfocusonlowerextremityfunctionandondifficultieswithmobility
Occupationaltherapistsaddressupperextremitydysfunctionanddifficultiesinactivitiesofdailyliving
Rehabilitationnursesareconcernedwiththeissuesofbowelandbladderdysfunctionandthemanagementofpressure
ulcers
Psychologistsdealwiththeemotionalandbehaviouralconcernsofthenewlyinjuredpatientandwithanypotential
cognitivedysfunction
Speechlanguagepathologistsaddresswithissuesofcommunicationandswallowing
Casemanagersandsocialworkersaretheprimaryinterfacebetweentherehabilitationteam,thepatientandhisorher
family,andthepayersource

FindingsonNervousSystemExamination
Twomaintypesoflesionsupperandlowermotorneuronsaredistinguishedinspinalcorddisorders.Itisimportantto
rememberthataspinalcordlesioncausesLMNsignsatthelevelofthelesionandUMNsignsbelowthatlevel.

ThispatienthasaspinalcordlesionatthelevelofC6.
Higherfunctionsandcranialnervesarenormal
LowestlevelofnormalsensationC6dermatomesbilaterally
LowestlevelofnormalmusclepowerC6(wristextension)
Atrophic,flaccidtricepswithfasciculations
Absentsupinatorandtricepsjerk(C7,C8)
Weakness,Spasticity,hyperreflexiaandupgoingplantarsinbothlowerlimbs,noobservedlowerlimbatrophyor
fasciculations

Gradingofmusclestretchreflexes
Byconventionreflexresponsesaregraded:
0
absent
+
Presentbutreduced
++
normal
+++
Increased,possiblynormal
++++
Greatlyincreased,oftenassociatedwithclonus

LowerMotorNeurons
Thesenervecells(themotorcellconcernedwithstriatedskeletalmuscleactivity)intheanteriorgraycolumnofthespinal
cordorbrainstemhaveaxonsthatpassbywayofthecranialorperipheralnervestothemotorendplatesofthemuscles.
Lowermotorneuronsareconsideredthefinalcommonpathwaybecausemanyneuralimpulsesfunnelthroughthemtothe
muscle;thatis,theyareactedonbythecorticospinal,rubrospinal,olivospinal,vestibulospinal,reticulospinal,and
tectospinaltractsaswellasbyintersegmentalandintrasegmentalreflexneurons.
Lesionsofthelowermotorneuronscanbelocatedinthecellsoftheanteriorgraycolumnofthespinalcordorbrainstem
orintheiraxons,whichconstitutetheventralrootsofthespinalorcranialnerves.Signsoflowermotorneuronlesions

19

includeweakness,flaccidparalysisoftheinvolvedmuscles,decreasedmuscletone,muscleatrophywithfasciculationsand
degenerationofmusclefibersovertime.Reflexesoftheinvolvedmusclearediminishedorabsent.

UpperMotorNeurons
Theuppermotorneuronisacomplexofdescendingsystemsconveyingimpulsesfromthemotorareasofthecerebrum
andsubcorticalbrainstemtotheanteriorhorncellsofthespinalcord.Itisessentialfortheinitiationofvoluntarymuscular
activity.Thetermitselfisusedmainlytodescribeneuronswithbodiesrostraltothoseoflowermotorneuronsinthespinal
cordorbrainstem,andtheirdescendingaxons.Onemajorcomponent,thecorticospinaltract,arisesinthemotorcortex,
passesthroughtheinternalcapsuleandbrainstem,andprojectswithinthespinalcordtothelowermotorneuronsofthe
cord.Anothercomponent,thecorticobulbartract,projectstothebrainstemnucleiofthecranialnervesthatinnervate
striatedmuscles.Uppermotorneuronscontrolvoluntaryactivation(butnotnecessarilyreflexactivation)oflowermotor
neurons.
Lesionsinthedescendingmotorsystemscanbelocatedinthecerebralcortex,internalcapsule,cerebralpeduncles,brain
stem,orspinalcord.Signsofuppermotorneuronlesionsinthespinalcordincludeparalysisorparesis(weakness)ofthe
involvedmuscles,increasedmuscletone(hypertonia)andspasticity,hyperactivedeepreflexes,noorlittlemuscleatrophy
(atrophyofdisuse),diminishedorabsentsuperficialabdominalreflexes,andabnormalreflexes(eg,Babinski'sresponse).
TheBabinskireflex(alsotermedthe"extensorplantar"response)suggestsdysfunctionofthecorticospinalsystem,
althoughitdoesnot,initself,telltheexaminertherostrocaudallocation(spinalcordvs.brainstemvs.cerebrum)ofthe
lesion.

FromWaxmanSClinicalNeuroanatomy,Chapter5TheSpinalCordLesionsinMotorPathways
http://www.accessmedicine.com.ezproxy.library.uq.edu.au/content.aspx?aID=5272117

SensorySystem

Painandtemperaturefibresenterthespinalcordviathedorsalnerverootandcrossafewsegmentshighertotheopposite
SpinothalamicTract,alsocalledtheventrolateral(oranterior)system.Thesespinothalamictractsactuallyconsistoftwo
adjacentpathways:Theanteriorspinothalamictractcarriesinformationaboutlighttouch,andthelateralspinothalamic
tractconveyspainandtemperature.Thesetractsascendtothebrainstem.
TheDorsalColumnTractsconveywelllocalizedsensationsoffinetouch,vibration,twopointdiscrimination,and
proprioception(positionsense)fromtheskinandjoints;theyascend,withoutcrossing,inthedorsalwhitecolumnofthe
spinalcordtothelowerbrainstem,crossingpriortothethalamus.

FromWaxmanSClinicalNeuroanatomy,Chapter5TheSpinalCordLesionsinMotorPathways
http://www.accessmedicine.com.ezproxy.library.uq.edu.au/content.aspx?aID=5272117

Trigger1.4

ONGOINGMANAGEMENT

AftertwoweeksinthespinalinjuryunititisnotedthatBensskinoverhissacrumisbecomingredandconcernisraised
thathemaybedevelopingapressurearea.Assessmentismadeofhischairandsittingpositionandchangesaremade
tohiscushion.

DiscussionPoints
1. Whatarethekeypointsinthemanagement?
Twoweeksinspinalinjuryunit
Redsacralskin?pressurearea
Assessmentandappropriatemanagement
2. Whatarepressureareas?Whatistheiraetiologyandhowcantheybeavoided.
3. Arespinalinjurypatientsatriskofothercomplications?
4. WhatisaDeepVenousThrombosis(DVT)?WhataretherisksforDVTandwhyarespinalinjurypatientsatparticular
risk?

NotesforTutors
Whatarethecausesofpressureareas?Howcantheybeavoided?
Thisisanimportantcomponentofbasicmedicalcareforanypatient.

20

Pressureareasareareasofdamageofskinandunderlyingtissuesduetounrelieveddirectpressureorshear.Theyoften
developoverbonyprominencesascompressiveforcesarenotamelioratedbysofterunderlyingtissues.
Pressureareasareoftenseeninpeoplewithneurologicinjurywhohavebodypartswhichremainimmobileand/or
insensate.Peoplewhoarephysiologicallyimpairedareatespeciallyhigherrisk.
Pressureareasremainariskforpeoplewithspinalinjuryfortherestoftheirlives.
Pressureareasarepreventedbygoodpositioningofbodypartsandregularmovementtopreventonebodypartbearing
continuouspressureloads.Goodskincareandvigilanceareextremelyimportantfactorsaswellasearlydetectionand
treatmentofanyareainwhichitmayappearthatapressureareaisdeveloping.Theycancausemajormorbidity.Ifa
persondevelopsapressurearea,theprimetreatmentisstrictrestoftheareainvolved.Thismayrequiresomerestriction
ofmobilityresultinginmajorimpairmentofsocialfunctioning.

Factorscontributingtopressureulcersaresummarizedbelow.
Pathomechanicalfactors(extrinsicorprimary)includethefollowing:
Compression
Maceration
Immobility
Pressure
Friction
Shear

Pathophysiologicfactors(intrinsicorsecondary)includethefollowing:
Fever
Anaemia
Infection
Ischemia
Hypoxemia
Malnutrition
Spinalcordinjury
Neurologicdisease
Decreasedleanbodymass
Increasedmetabolicdemands

Whatothermajormedicalproblemarepeoplewithpoormobilityatriskof?

AnothermajorriskforpeoplewhoareimmobileisDeepVenousThrombosis.
Clottingoccursinthemajorveinsespeciallyinthepelvisandlowerlimbs.Thisclotcanbreakoffandembolisetothelungs
causinglifethreateningpulmonaryembolus.
DeepVenousThrombosisisaconditionassociatedwith
(1)venousstasis,
(2)activationofbloodcoagulation,and
(3)veindamage.
ThesefactorshavecometobeknownastheVirchowtriad.

AllthreeoccurafterspinalinjuryandpreventionofDVTisanimportantfactorespeciallyinearlyhospitalizationpostinjury.

Neurologicdeterioration,aspirationandpulmonarycomplications,sepsis,autonomicdysreflexiaandurinarytractinfection
areothercomplications.

Trigger2.1

DISCHARGEPLANNING

It has now been six months since his accident and with intensive rehabilitation in the spinal unit Ben is able to
independentlyfeedandgroomhimself,requiringassistancewithdressing,bathingandtransfer.Ben,hisfamilyandthe
spinalinjuryunitteamdiscussdischargefromhospitalandindependentliving.
ClosefollowupofBensprogresswillbeprovided.

21

DiscussionPoints
1.

2.
3.
4.
5.

WhatarethekeypointsregardingBensdischargefromthespinalinjuryunit?
Planningfordischarge
Majorlifestylechanges
Modificationstohomeetc
Ongoingcareandfollowup
Whatisanappropriateleveloffunctioningfordischargefromthespinalinjuriesunit?
FromwhatyouunderstandofhisneurologicallesionswhatactivitiesofdailylivingwouldyouexpectBentobeableto
undertakeindependently?
WhatADLsmayherequireassistancewith?
Whatinterventions,treatmentsandaidsishelikelytorequire?

NotesforTutors
Whilegoalsmustbeindividualized,therearecertainexpectationsaccordingtoinjurylevelforhealthyindividualswith
spinalcordinjury(SCI)whohavereceivedrehabilitationtraining.ApersonwithtetraplegiawithinjuryabovethelevelofC5
isdependentuponothersforactivitiessuchasfeeding,dressing,andbathingandrequirestheavailabilityofanattendant
atalltimes.However,apoweredwheelchairofferssuchapersonindependenceinmobilityinanaccessibleenvironment
andindependenceinweightshifting.

PersonswithinjurylevelsofC5andC6haveincreasedfunctionalcapacitybutstillrequirephysicalassistanceforactivities
suchasdressing,bathing,andtransfers.ApersonwithaninjurylevelofC7maybeindependentwiththeproperequipment
inalloftheseareas,requiringonlysomeassistancewithbowelmanagement.Paraplegiaiscompatiblewithtotal
independenceatawheelchairlevel.However,eventheseindividualsmayrequiretheassistanceofahomemaker.

C6isthehighestlevelatwhichpatientscanhaveacompleteinjuryandstillfunctionindependentlywithouttheaidofan
attendant,althoughthissituationisnotcommon.Individualswithinjuriesatthislevelcanachievefunctionalindependence
intermsoffeeding,grooming,bathing,andbedmobilitybyusingassistivedevices.Theycandresstheirupperbodyand
assistwithlowerbodydressing,aswellaswiththebladderandbowelprogram.Withtheuseofaslideboard,personswith
C6tetraplegiamaybecomeindependentinperformingtransfersfromabedtoachair,althoughtheyusuallyrequire
assistancewiththese.Intermittentcatheterizationforbladdercaremaybepossiblewithsetupandassistivedevices,
althoughthisisnotcommonandistechnicallymoredifficultforwomenthanformen.

TheTransitionalRehabilitationProgram(TRP)isaninnovativeprogramwhichassistspeopleaffectedbyspinalcordinjury
inthetransitionfromhospitalrehabilitationtocommunityliving.Itoffersaflexiblerehabilitationservice,focussedon
individualgoals,andenablesearlierdischargefromhospital.TRPassistspeopletoconsolidateandbuildonskillsdeveloped
intheSpinalInjuriesUnitwiththesupportofanexperiencedteamofhealthprofessionals.Theinvolvementoffamily,
partnersandfriendsisactivelyencouragedintheseprograms.

TRPdeliversrehabilitationservicestoclientsoftheSpinalInjuriesUniteitherintheirownhomesorinahomelikesetting
outsideofthehospitalenvironment.Itallowsclientstoreestablishfamilyrelationshipsthathavebeendisruptedby
lengthyperiodsofhospitalisation.Itenablesthemtobegintoregainsomecontrolanddirectionintheirlivesandto'polish
off'thephysicalskillsneededtoliveathomeandincommunity.Itprovidesthemwithmoreasatisfactoryrehabilitation
environment,betterqualityoflifeandenhancedoutcomes.

TheTRPisstaffedbyadedicatedmultidisciplinaryteamconsistingofNursing,Physiotherapy,OccupationalTherapy,and
SocialWorkprofessionals.PersonalCareAssistantsareemployedtoassistwithpersonalcaretasks.

Therearemajorpsychosocialfactorswhichcometobearinthecareofspinalinjurypatients.TheseminarheldonTuesday
discussedtheseindepth.Areviewofthemajorthemeswouldbeusefulatthispoint.

Trigger3.1

CLOSURE:

OneyearlaterBencontinueswithhisrehabilitationprogram,strugglingtoadjusttohisnewlife.Heisretrainingtowork
asacallcentreoperator.Heasks,Willitevergetanybetterthanthis?

22


Discussionpoint
DiscusspossiblelongtermhealthconsequencesforBen.Istherethepotentialforfurtherrecovery?

Additionalnotesfortutors

Neurologicrecoverycanbedividedinto2categories:(1)recoverywithinthezoneofinjuryand(2)recoverybelowthezone
of injury. The zone of injury is typically considered the first 3 abnormal dermatomes or myotomes. Muscles that are
completely plegic at the time of injury within the zone of injury have a fair possibility of regaining some motor power,
althoughthispowertypicallyisnonfunctional.Musclesthathadevenasmallamountofcontractionatthetimeofinjury
haveaverygoodpossibilityofattainingfunctionalmotorpower.

ImprovementfollowingSCImaybemediatedinpartbyrecoveryofpartiallydamagedneurons.Inaddition,recoveryatthe
levelofinjurymayoccurbecauseofperipheralsproutingofsparedneurons.Distalrecoveryfollowingincompletelesions
maybemediatedbyreceptorupregulationandbyanexpansionofsynapticfields,allowinganincreaseintheinfluenceof
sparedpathways.Asimilarmechanismmayunderliethedevelopmentofspasticity.
Themoreincompletetheinjuryis,especiallyoninitialexaminationat72hoursto1weekaftertheinjuryhasoccurred,the
morefavourablethepotentialforneurologicrecovery.

Neurologicrecoveryusuallyplateausinthefirst36months(althoughchangeshavebeenreported>1yearafterinjury).
Individuals with motorcomplete injuries are usually expected to recover 1 motor level of function distal to the lowest
motorlevelobservedduringtheirinitialexamination.

Lifeexpectancyforpatientswithspinalcordinjurycontinuestoincreasebutarestillbelowthegeneralpopulation.The
leading causes of death in patients following SCI are pneumonia and other respiratory conditions, followed by heart
disease, subsequent trauma, and septicaemia. Suicide and alcoholrelated deaths are also major causes of death in
patientswithSCI.

23