Orthopaedic Neurology: A Diagnostic Guide to Neurologic Levels

OrthopaedicNeurologyADiagnosticGuidetoNeurologicLevels

SecondEdition

J.D.Hoppenfeld,MDInterventionalPainManagementMedicalDirectorSoutheastPain&SpineCareCharlotte,NorthCarolina

StanleyHoppenfeld,MDClinicalProfessorofOrthopedicSurgery(Retired)AlbertEinsteinCollegeofMedicineBronx,NewYork

IncollaborationwithRichardHutton

MedicalillustrationsbyHughThomasandBernieKida

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Secondedition

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Names:Hoppenfeld,Stanley,1934-author.|Hoppenfeld,J.D.(Jon-David),author.Title:Orthopaedicneurology:adiagnosticguidetoneurologiclevels/J.D.Hoppenfeld,StanleyHoppenfeld;incollaborationwithRichardHutton;medicalillustrationsbyHughThomas.Description:Secondedition.|Philadelphia:WoltersKluwerHealth,[2018]|StanleyHoppenfeld’snameappearsfirstonpreviousedition.|Includesbibliographicalreferencesandindex.Identifiers:LCCN2017042946|ISBN9781496360670Subjects:|MESH:SpinalCordDiseases—diagnosis|NeurologicExamination—methods|SpinalNerveRootsClassification:LCCRC400|NLMWL402|DDC616.8/3—dc23LCrecordavailableat

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Dedication

Tomywife,Brie,andmychildren,PalmerandEmery.Youaddfulfillmenttomylifedaily.

Tomyfather,whotaughtmetheimportanceofthephrasethatprecededallofhisbooks,“Toallthepeoplewhopreservedthisbodyofknowledge,addedtoitandpasseditonforanothergeneration.”Tomymotherforhercontinuedloveandsupport.

TomycolleaguesatSoutheastPain&SpineCare.Thelevelatwhichyoutakecareofourpatientsonadailybasisexemplifiesthebestinmedicine.

ToDr.BrandonValentineforhisreviewoftheupperextremitychapter.

TotheNYUDepartmentofNeurology,whichprovidessuperbtrainingandawonderfulenvironmenttogrow.

TotheChicagoMedicalSchool.J.D.Hoppenfeld

Tomyfamily.StanleyHoppenfeld

Preface

Whiletheyearshavepassedsincethefirsteditionofthisbook,basicanatomyhas not. This book reflects improvements in medical illustration as well asteachingtechniques.Theupdatedversionmakeslearninganatomymoresimpleandclear.Advancesinhowwediagnoseandtreatpatientswithspinal injuriesarereflectedintheupdatedtextaswell.

J.D.Hoppenfeld

PrefacetothePreviousEdition

Years ago, I felt the need for a manual that would reduce the diagnosis ofneurologiclevelstoitscommondenominatorsandcombinethemwiththebasicprinciplesofneurology toassist in theappraisalof spinalcordandnerve rootproblems.Asthebookbegantotakeshapeinmymind,itbecameapparentthatthe most important aspects of transmitting this information would lie in itsorganizationandtheclarityofillustrations.Thefinalstructurewouldhavetobesimpleandclear,containingthematerialessentialtoteachthecrucialconceptsofexaminationanddiagnosis.

Thisbookhasbeenwrittenforthosewhowishtounderstandmoreclearlytheclinicalconceptsbehindneurologic levels. Ithasbeendesigned tobereadsequentially, from cover to cover. Each chapter presents basic neurologicinformation first, and then gives it clinical significance by applying it to thediagnosisofthemorecommonneurologicpathologies.Thepatternofteachingthusmoves from concept to practice and from the general rule to its specificapplication.

However,clinicalexperienceremainsthekeytorealunderstanding.Abookcan do no more than present, clearly and concisely, suggested methods ofevaluation.Intheinterestofsuchclarity,someoftheinformationpresentedherehas been simplified. The clinical findings for each neurologic level have, forexample,beenstylizedtomakebasicconceptsandfactseasiertounderstand;itmustbeclinicalexperiencethatuncoversthevariationsandexceptionsthatariseinindividualpatients.AsGoethesaid,“Whatoneknows,onesees.”

ThisbookisanexpressionofmyteachingexperienceattheAlbertEinsteinCollege of Medicine, where I have watched orthopaedic, neurosurgical,neurologic,physicalmedicine,andfamilypracticeresidents,aswellasphysicaltherapists,seekthisknowledge.Ihopethisinformation,andthespecialwayinwhich it is organized, provide the understanding necessary to assess theinvolvementofneurologiclevels.

StanleyHoppenfeld

Acknowledgments

Richard Hutton for his loyalty and devotion to this project. His personalfriendship,senseoforganization,andknowledgeoftheEnglishlanguagehelpedmake this book possible. Hugh Thomas for his exceptionally fine art work,which illustrates this book.Hispersonal friendshipover theseyears is greatlyappreciated.

Tomyfellowattendingsat theAlbertEinsteinCollegeofMedicine,whohavebeenverysupportiveduringthewritingandteachingofthismaterial:UrielAdar,DavidM.Hirsh,RobertSchultz,EliasSedlin,andRashmiSheth.TotheBritishFellows,whohaveparticipatedintheteachingoforthopaedicneurologyduring their staywith us at “Einstein”:CliveWhalley,Robert Jackson,DavidGruebel-Lee, David Reynolds, Roger Weeks, Fred Heatley, Peter Johnson,RichardFoster,KennethWalker,MaldwynGriffiths, JohnPatrick, andRobertJohnson. To the orthopaedic residents of the Albert Einstein College ofMedicine,forallowingmethepleasureofteachingthismaterial.

Hospital forJointDiseases,whichawardedmetheFrauenthalFellowshipand gave me world exposure to problems of the spine. Rancho Los AmigosHospital for the education I received in the areas of paraplegia and children’sspinaldeformities.LodgeMoorParaplegicCenter,wherealargeamountofmyexperienceindealingwithparaplegicpatientswasobtained.

MaldwynGriffith,whotookthetimetohelpusreorganizethemanuscript,breathing new life into it. John Patrick, for helping me by reviewing themanuscriptmany times,makingpositivesuggestions,andhelping toprepareaproper bibliography. Al Spiro for taking the time to review the manuscript,making many valuable suggestions, and upholding the special viewpoint ofpediatricneurology.GabriellaMolnarindeepappreciationforherreviewoftheinitial manuscript, for her positive suggestions, and for reviewing the finalmanuscript. Arthur Abramson in appreciation for his detailed review of theparaplegic and tetraplegic sections. He provided a mature sounding boardagainstwhichIhavetestedmanyideas.EdDelagiforreviewingthemanuscriptandbeinga friendwhenonewasneeded.CharlotteShelby inappreciationfor

her review of the manuscript and editorial suggestions during that wonderfulCaribbeancruise.

VictorKligforallofhishelpindevelopingtheelectronicspinalbraceandevaluatingneurologicinnervationtotheparaspinalmuscles.PaulHarringtonforhisbrillianceinthesurgicalapproachtothespineandformakingmeappreciatehowtoimprovespinalalignment,makingmanypatient’slivesfullerandricher.W. J. W. Sharrard in appreciation for the time he spent with me during myfellowshipinSheffield.Myknowledgeofmeningomyelocelechildrenisbasedonhisteachingaswellasmostofmyunderstandingofneurologiclevels,fromhis basic research of anterior horn cell involvement in patients withpoliomyelitis. The late Sir Frank Holdsworth for the time he spent with mediscussing spinal problems duringmy visit to Sheffield.My understanding ofspine stability isbasedonhiswork.Mr.EvansandMr.HardyofSheffield inappreciation for their time spent with me at the Paraplegic Center. JacquelinPerry,who,duringmyfellowship,spentmanyhourseducatingmeintheareasof paraplegic and children’s deformities. Herman Robbins, who, during myresidency, emphasized the neurologic evaluation of patients with spinalproblems.EmanuelKaplan for opening thedoor to neurology for orthopaedicsurgeons by translating Duchenne’s textbook, Physiology of Motion, intoEnglishandfortakingthetimetoinstructmeinthesematters.BenGolub,whohastakenthetimetoevaluatespinesandpassedthisspecialknowledgeontoalloftheresidentstaff.AlexNormanforhisspecialteachingsinradiologyofthespine.AlBetcher for teachingmeneurologic level evaluationofpatientswithspinalanesthesia.JoeMilgramforallofhishelpduringandaftermyresidencyattheHospitalforJointDiseases.

AlfNachemson,mylong-termfriend,withwhomIhavespentmanyhoursdiscussing spinal problems. Nathan Allan andMimi Shore, my personal andprofessional friends, who have consistently shared their professional andpractical knowledgewithme.AlGrant andLynnNathanson for their help inrunning the Meningomyelocele Service. To my neurosurgical colleagues, inparticularKenShulman,StephenWeitz,andHughRosomoff,withwhomIhavehad the pleasure of sharing patient care, surgery, and numerous discussionsabout neurologic level problems.Roberta andDavidOzerkis for a lifetime offriendshipandhelp.FrankFerrieriforhisfriendshipandsupport.

ArthurandWildaMerker,myfriends.Someofthewritingofthisbookwasdone at their lovely home by the sea.Muriel Chaleff, who, through personalefforts, provided a professional touch in preparing this manuscript. Lauretta

White, who was most devoted in the preparation of this manuscript. AntheaBlamire,whowasagreathelpinthetypingofthismanuscript.LewReinesforhishelpinhandlingthefirstedition’smanuscriptandproduction.FredZellerinhelping to arrange for the first edition’s distribution throughout the world.BrooksStewartforhishelpinconvertingamanuscriptandtakingittoitsfinalform.Toourpublisher,J.B.LippincottCompany,whohasbroughtthisprojecttoasuccessfulconclusion.

Contents

IntroductionMotorPowerSensationReflex

Part1 NerveRootLesionsbyNeurologicLevel

1EvaluationofNerveRootLesionsInvolvingtheUpperExtremityTestingofIndividualNerveRoots:C5-T1NeurologicLevelC5NeurologicLevelC6NeurologicLevelC7NeurologicLevelC8NeurologicLevelT1Summary

ClinicalApplicationofNeurologicLevelsHerniatedCervicalDisksCervicalNeckSprainversusHerniatedDiskTheUncinateProcessesandOsteoarthritisNerveRootAvulsions

2EvaluationofNerveRootLesionsInvolvingtheTrunkandLowerExtremity

TestingofIndividualNerveRoots,T2-S4NeurologicLevelsT2-T12NeurologicLevelsT12-L3

NeurologicLevelL4NeurologicLevelL5NeurologicLevelS1NeurologicLevelsS2-S4Summary

ClinicalApplicationofNeurologicLevelsHerniatedLumbarDisksLowBackDerangementversusHerniatedDiskSpondylolysisandSpondylolysthesisHerpesZosterPoliomyelitis

Part2 SpinalCordLesionsbyNeurologicLevel

3CervicalCordLesions:TetraplegiaEvaluationofIndividualCordLevels:C3-T1NeurologicLevelC3(C3Intact)NeurologicLevelC4(C4Intact)NeurologicLevelC5(C5Intact)NeurologicLevelC6(C6Intact)NeurologicLevelC7(C7Intact)NeurologicLevelC8(C8Intact)NeurologicLevelT1(T1Intact)UpperMotorNeuronReflexes

ClinicalApplicationFracturesandDislocationsoftheCervicalSpineActivitiesofDailyLivingHerniatedCervicalDisksTumorsoftheCervicalSpineTuberculosisoftheSpineTransverseMyelitis

4SpinalCordLesionsBelowT1,IncludingtheCaudaEquinaParaplegiaNeurologicLevelsT1-T12L1NeurologicLevel(L1Intact)L2NeurologicLevel(L2Intact)L3NeurologicLevel(L3Intact)L4NeurologicLevel(L4Intact)L5NeurologicLevel(L5Intact)S1NeurologicLevel(S1Intact)

UpperMotorNeuronReflexesPathologicReflexesNormalSuperficialReflex

ClinicalApplicationFurtherEvaluationofSpinalCordInjuriesHerniatedThoracicDisks

EvaluationofSpinalStabilitytoPreventFurtherNeurologicLevelInvolvementDiagnosisFlexionInjuryFlexion-RotationInjuryHyperextensionInjuriesCompressionInjuries

5MeningomyeloceleDeterminationofLevelL1-L2NeurologicLevel(L1IsIntact,L2IsNot)L2-L3NeurologicLevel(L2IsIntact,L3IsNot)L3-L4NeurologicLevel(L3IsIntact,L4IsNot)L4-L5NeurologicLevel(L4IsIntact,L5IsNot)L5-S1NeurologicLevel(L5IsIntact,S1IsNot)

S1-S2NeurologicLevel(S1IsIntact,S2IsNot)S2-S3NeurologicLevel(S2IsIntact,S3IsNot)

MilestonesofDevelopmentSittingStandingWalking

UnilateralLesionsHydrocephalusExaminationoftheUpperExtremitySuggestionsforExaminationofthePatientwithMeningomyelocele

Introduction

Thespinalcordisdividedintosegments.Nerverootsexitthespinalcordateachsegmentallevelandarenumberedinrelationtothelevelfromwhichtheyexit.There are 8 cervical, 12 thoracic, 5 lumbar, and 5 sacral nerves. The C5-T1segments innervate the upper extremity, and the T12-S4 segments the lowerextremity;thesetwosectionsofthecordhavethegreatestclinicalsignificance.

Pathology affecting the spinal cord and nerve roots commonly producessymptoms and signs in the extremities according to the specific neurologiclevelsinvolved.Theselevelscanusuallybediagnosedclinically,becauseeachlevelofinjuryhasitsowncharacteristicpatternofdenervation.

The commondenominator in injuries to either the cordor thenerve rootliesinthesegmentalpatternofalterationofmotorpower,sensation,andreflexin theextremities.Evaluationof the integrityof theneurologic levelsdependson a knowledge of the dermatomes, myotomes, and reflexes. Differentdermatomes(areasofsensationontheskinsuppliedbyasinglespinalsegment)andmyotomes (groups ofmuscles innervated by a single spinal segment) areaffected depending upon the level involved and upon whether the pathologyinvolves thecordor thenerve rootsemanating from it. It is throughaclinicalevaluationofmotorpower,sensation,andreflexthatthecorrectneurologiclevelofinvolvementcanbeestablished.

MotorPowerTheimpulsesthatsupplymotorpoweraretransportedinthespinalcordviathelong tracts and, in particular, via the corticospinal tracts. Interruption of thenerverootcausesdenervationandparalysisofitsmyotome;interruptionofthetractcausesspasticparalysis(Fig.I-1).Pressureonthenerverootmayproduceadecrease inmusclestrength thatcanbeevaluatedbest through thestandardssetbytheNationalFoundationofInfantileParalysis,Inc.,CommitteeonAfter-Effects, and adopted by the American and British Academies of Orthopaedic

Surgeons(TableI-1).Inlearningtogradeamuscle,itisbesttorememberthatagrade3muscle

canmove the joint through a range ofmotion against gravity.Above grade 3(grades4and5),resistanceisaddedtothemuscletest;belowgrade3(grades2,1,and0),gravityiseliminatedasafactor.

Muscletestingshouldberepeatedonaregularbasistodeterminewhetherthelevelofthelesionhaschangedandcreatedeitherfurthermuscularparalysisor improvement. Repetitive muscle testing against resistance helps determinewhether the muscle fatigues easily, implying weakness and neurologicinvolvement.

FIGUREI-1Thecorticospinalandspinothalamictracts.

TABLEI-1MUSCLEGRADINGCHARTMUSCLEGRADATIONS DESCRIPTION5–Normal Completerangeofmotionagainstgravitywithfullresistance4–Good Completerangeofmotionagainstgravitywithsomeresistance3–Fair Completerangeofmotionagainstgravity2–Poor Completerangeofmotionwithgravityeliminated1–Trace Evidenceofslightcontractility.Nojointmotion0–Zero Noevidenceofcontractility

Sensation

Sensation of pain and temperature is carried in the spinal cord via the lateralspinothalamic tract,whereas touch iscarried in theventral spinothalamic tract(Fig.I-1).Pathologytothecordornerverootresultsinthelossoflighttouch,followedbylossofsensationofpain.Duringarecoveryfromnerverootinjury,sensation of pain returns before light touch. The two sensations are testedseparately,lighttouchwithacottonswabandpainwithpinpricks.

Whentestingforpain,useapininagentlestickingmotion.Thepinpricksshould follow in succession, but not too rapidly. A pinwheel is an excellentalternativemethodofevaluatingalterationsinsensation,becausetwoneurologicpinwheels can be used simultaneously, one on each side, to permit bilateralcomparison. Safety pins may also be used. The use of needles is notrecommended because they have cutting surfaces andmay injure the patient.Onceanareaofalteredsensationisfound,itcanbelocatedmorepreciselybyrepeated testing from the area of diminished sensation to the area of normalsensation. Sensation tests depend largely on subjective responses; fullcooperationofthepatientisnecessary.

Aftersensationisevaluated,theresultsshouldberecordedonadermatomediagram as normal, hyperesthetic (increased), hypesthetic (decreased),dysesthetic(altered),oranesthetic(absent).

ReflexThestretchreflexarciscomposedofanorgancapableofrespondingtostretch(musclespindle),aperipheralnerve(axon),thespinalcordsynapse,andmusclefibers (Fig. I-2). Impulses descend from the brain along long (upper motorneuron) tracts tomodulate the reflex.As ageneral rule, an interruption in thebasicreflexarcresultsinthelossofreflex,whereaspressuresonthenerverootitselfmaydecreaseitsintensity(hyporeflexia).Interruptionoftheuppermotorneuron’s regulatory control over the reflexwill ultimately cause it to becomehyperactive(hyperreflexia).

Reflexes should be reported as normal, increased, or decreased, anevaluationwhich requires that one side be comparedwith the other. Bilateralcomparison provides a direct, immediately accessible way to detect anyalteration in reflexes and is essential for an accurate diagnosis of pathologybecausethedegreeofreflexactivityvariesfrompersontoperson.

Theconceptofdeterminingneurologic levelsapplies to theevaluationof

spinal injuries, developmental anomalies, herniated discs, osteoarthritis, andpathologicprocessesof thecord itself.All thesepathologicprocessesresult inspecificsegmentaldistributionofneurologicsignsintheextremitiesbecauseoftheirdirecteffectonthespinalcordandnerveroots.

FIGUREI-2Thestretchreflexarc.

Note that thedifference infindingsbetweencordornerverootpathologyandperipheralnerveinjuriesisreflectedindifferencesinthedistributionoftheneurologic findings of motor power, sensation, and reflex. Although eachdermatomeandmyotomeisinnervatedatacordlevelandbyaperipheralnerve,eachhasitsowndistinctpatternofinnervation.

NerveRootLesionsbyNeurologicLevel

EvaluationofNerveRootLesionsInvolvingtheUpperExtremity

Examination by neurologic level is based on the fact that the effects ofpathologyinthecervicalspinearefrequentlymanifestedintheupperextremity(Fig.1-1).Problems that affect the spinal cord itselfornerve roots emanatingfromthecordmaysurfaceintheextremityasmuscleweaknessorabnormality,reflex abnormality, and sensory diminution; the distribution of neurologicfindingsdependson the level involved.Thus,a thoroughneurologic testingoftheextremityhelpsdetermineanyinvolvementofneurologiclevels;itmayalsoassistintheevaluationofanassortmentofproblemsoriginatinginthecervicalcordoritsnerveroots.

The following diagnostic tests demonstrate the relationship betweenneurologicproblemsintheupperextremityandpathologyinvolvingthecervicalnerve roots. For each neurologic level of the cervical spine, motor power,reflexes,andareasofsensationintheupperextremityshouldbetested,sothatthelevelinvolvedcanbeidentified.Wehavebegunindividualnerveroottestingwith C5, the first contribution to the clinically important brachial plexus.AlthoughC1-C4arenotincludedinourtestsbecauseofthedifficultyoftestingthem,itiscrucialtorememberthattheC4segmentisthemajorinnervationtothediaphragm(viathephrenicnerve).

FIGURE1-1Thecervicalspine.

TestingofIndividualNerveRoots:C5-T1NeurologicLevelC5

MuscleTestingThe deltoid and biceps are the two most easily tested muscles with C5innervation.ThedeltoidisalmostapureC5muscle;thebicepsisinnervatedbybothC5andC6,andevaluationofitsC5innervationmaybeslightlyblurredbythisoverlap(Fig.1-2).

FIGURE1-2NeurologiclevelC5.

Deltoid:C5(AxillaryNerve):Thedeltoidisactuallyathree-partmuscle.Theanteriordeltoidflexes,themiddledeltoidabducts,andtheposteriordeltoidextendstheshoulder;ofthethreemotions,thedeltoidactsmostpowerfullyinabduction(Fig.1-2).Becausethedeltoiddoesnotworkaloneinanymotion,itmaybedifficulttoisolateitforevaluation.Therefore,noteitsrelativestrengthinabduction,itsstrongestplaneofmotion(Fig.1-3).Primaryshoulderabductors(Fig.1-4):1. Supraspinatus

C5,C6(suprascapularnerve)2. Deltoid(middleportion)

C5,C6(axillarynerve)Secondaryshoulderabductors:

1. Deltoid(anteriorandposteriorportions)2. Serratus anterior (by direct stabilizing action on the scapula, because

abductionoftheshoulderrequiresastablescapula).Standbehindthepatientandstabilizetheacromion.Slideyourstabilizing

handslightly laterally so that,whileyoustabilize theshouldergirdle,youcanalsopalpatethemiddleportionofthedeltoid.

Instructthepatienttoabducttheirarmwiththeelbowflexedto90°.Asthepatientmovesintoabduction,graduallyincreaseyourresistancetotheirmotionuntil you have determined themaximum resistance the patient can overcome(Fig.1-5). Record your findings in accordancewith themuscle grading chart(seepage2).

Biceps:C5-C6(MusculocutaneousNerve):Thebicepsisaflexoroftheshoulderandelbowandasupinatoroftheforearm(Fig.1-6);tounderstanditsfullfunction,envisionamandrivingacorkscrewintoabottleofwine(supination),pullingoutthecork(elbowflexion),anddrinkingthewine(shoulderflexion)(Fig.1-7).

FunctionoftheThreePartsoftheDeltoidMuscle

FIGURE1-3Eachheadofthedeltoidanditsfunction.

FIGURE1-4AShoulderabduction.

FIGURE1-4BDeltoid.Origin:Lateralthirdofclavicle,uppersurfaceofacromion,spineofscapula.Insertion:Deltoidtuberosityofhumerus.

FIGURE1-4CSupraspinatus..Origin:Supraspinousfossaofscapula.Insertion:Superiorfacetofgreatertuberosityofhumerus,capsuleofshoulderjoint.

Todetermine theneurologic integrityofC5,weshall test thebicepsonlyfor elbow flexion.Because thebrachialismuscle, theothermain flexorof theelbow, is also innervated by C5, testing flexion of the elbow should give areasonableindicationofC5integrity.

Totestflexionoftheelbow,standinfrontofthepatient,slightlytowardthesideoftheelbowbeingtested.Stabilizehisupperextremityjustproximaltotheelbowjointbycuppingyourhandaroundtheposteriorportionoftheelbow.Theforearmmust remain in supination to preventmuscle substitution,whichmayassistelbowflexion.

Instruct thepatient to flexhisarmslowly.Applyresistanceas thepatientapproaches 45° of flexion; determine themaximum resistance that the patientcanovercome(Fig.1-8).

ReflexTestingBicepsReflex:ThebicepsreflexispredominantlyanindicatorofC5neurologicintegrity;italsohasasmallerC6component.Notethat,becausethebicepshastwomajorlevelsofinnervation,thestrengthofthereflexneedstobeonlyslightlyweakerthanthestrengthoftheoppositesidetoindicatepathology.Itisessentialtocompareoppositesidesofthebody.

FIGURE1-5Muscletestforshoulderabduction.

To test the reflex of the bicepsmuscle, place the patient’s arm so that itrests comfortably across your forearm.Your hand should be under themedialsideoftheelbow,actingassupportforthearm.Placeyourthumbonthebicepstendoninthecubitalfossaoftheelbow(Fig.1-9).Tofindtheexactlocationofthe biceps tendon, have the patient flex his elbow slightly.The biceps tendon

willstandoutunderyourthumb.Instructthepatienttorelaxtheextremitycompletelyandtoallowittorest

onyourforearm,withtheelbowflexedtoapproximately90°.Withthenarrowend of a reflex hammer, tap the nail of your thumb. The biceps should jerkslightly,amovementthatyoushouldbeabletoeitherseeorfeel.ToremembertheC5reflexlevelmoreeasily,notethatwhenthebicepstendonistapped,fivefingerscomeupinauniversalgestureofdisdain(Fig.1-9).

FIGURE1-6AElbowextensionandflexion.

FIGURE1-6BBicepsbrachii(left).Origin:Shortheadfromtipofcoracoidprocessofscapula,longheadfromsupraglenoidtuberosityofscapula.Insertion:Radialtuberosityandbylacertusfibrosustooriginsofforearmflexors.FIGURE1-6CBrachialis(right).Origin:Lowertwo-thirdsoftheanteriorsurfaceofthehumerus.Insertion:Coronoidprocessandtuberosityoftheulna.

SensationTestingLateralArm(AxillaryNerve):TheC5neurologiclevelsuppliessensationtothe

lateralarm,fromthesummitoftheshouldertotheelbow.Thepurestpatchofaxillarynervesensationliesoverthelateralportionofthedeltoidmuscle.ThislocalizedsensoryareawithintheC5dermatomeisusefulforindicatingspecifictraumatotheaxillarynerveaswellasgeneraltraumatotheC5nerveroot(Fig.1-10).

FIGURE1-7Variousfunctionsofthebiceps.(Hoppenfeld,S.:PhysicalExaminationoftheSpineandExtremities.Norwalk,CT:Appleton-Century-Crofts,1976.)

FIGURE1-8Muscletestforthebiceps.

NeurologicLevelC6

MuscleTestingNeitherthewristextensorgroupnorthebicepsmusclehaspureC6innervation.ThewristextensorgroupisinnervatedpartiallybyC6andpartiallybyC7;thebicepshasbothC5andC6innervation(Fig.1-11).

FIGURE1-9ABicepsreflextest.FIGURE1-9BAneasywaytorememberthatthebicepsreflexisinnervatedbyC5istoassociatefivefingerswithneurologiclevelC5.

FIGURE1-10ThesensorydistributionoftheC5neurologiclevel.

WristExtensorGroup:C6(RadialNerve)

Radialextensors(Fig.1-12):1. Extensorcarpiradialislongusandbrevis,

Radialnerve,C6Ulnarextensor:1. Extensorcarpiulnaris2. C7

Totestwristextension,stabilizetheforearmwithyourpalmonthedorsumof the wrist and your fingers wrapped around it. Then instruct the patient toextend his wrist.When the wrist is in full extension, place the palm of yourresistinghandoverthedorsumofthehandandtrytoforcethewristoutofthe

extendedposition(Fig.1-13).Normally,youwillbeunabletomoveit.Testtheopposite side as ameans for comparison.Note that the radialwrist extensors,which supplymostof thepower forextension, are innervatedbyC6,whereasthe extensor carpi ulnaris is innervated primarily by C7. If C6 innervation isabsent and C7 is present, the wrist will deviate to the ulnar side duringextension.On the other hand, in a spinal cord injurywhereC6 is completelysparedandC7isabsent,radialdeviationwilloccur(Fig.1-14).

Biceps:C6(MusculocutaneousNerve):Thebicepsmuscle,inadditiontoitsC5innervation,ispartiallyinnervatedbyC6.Testthebicepsbymuscletestingflexionoftheelbow.(Fordetails,seepage11.)

FIGURE1-12AWristextensionandflexion.

FIGURE1-12BExtensorcarpiulnaris(left).Origin:Fromcommonextensortendonfromlateralepicondyleofhumerusandfromposteriorborderofulna.Insertion:Medialsideofthebaseofthe5thmetacarpalbone.FIGURE1-12CExtensorcarpiradialislongus(right).Origin:Lowerthirdoflateralsupracondylarridgeofhumerus,lateralintermuscularseptum.Insertion:Dorsalsurfaceofthebaseofthe2dmetacarpalbone.FIGURE1-12CExtensorcarpiradialisbrevis(right).Origin:Fromcommonextensortendonfromlateralepicondyleofhumerus,radialcollateralligamentofelbowjoint,and

intermuscularsepta.Insertion:Dorsalsurfaceofbaseof3dmetacarpalbone.

ReflexTestingBrachioradialisReflex:ThebrachioradialisisinnervatedbytheradialnerveviatheC6neurologiclevel.Totestthereflex,supportthepatient’sarmasyoudidintestingthebicepsreflex.Tapthetendonofthebrachioradialisatthedistalendoftheradius,usingtheflatedgeofyourreflexhammer;thetapshouldelicitasmallradialjerk(Fig.1-15).Testtheoppositesideandcompareresults.ThebrachioradialisisthepreferredreflexforindicatingC6neurologiclevelintegrity.

BicepsReflex:ThebicepsreflexmaybeusedasanindicatorofC6neurologicintegrityaswellasC5.However,becauseofthisdualinnervation,thestrengthofitsreflexneedonlyweakenslightlyincomparisontotheoppositesidetoindicateneurologicproblems.ThebicepsreflexispredominantlyaC5reflex.

FIGURE1-13Muscletestforwristextension.

Totestthebicepsreflex,tapitstendonasitcrossestheelbow.(Fordetails,

seepage11.)

SensationTestingLateralForearm(MusculocutaneousNerve):C6suppliessensationtothelateralforearm,thethumb,theindexfinger,andone-halfofthemiddlefinger.ToremembertheC6sensorydistributionmoreeasily,formthenumber6withyourthumb,index,andmiddlefingersbypinchingyourthumbandindexfingertogetherwhileextendingyourmiddlefinger(Fig.1-16).

NeurologicLevelC7

MuscleTestingAlthoughthetriceps,wristflexors,andfingerextensorsarepartiallyinnervatedbyC8,theyarepredominantlyC7muscles.Allofthesemotionscometogetherinthethrowingmotionofabaseball(Fig.1-17).

Triceps:C7(RadialNerve):Thetricepsistheprimaryelbowextensor(Fig.1-18).Totestit,stabilizethepatient’sarmjustproximaltotheelbowandinstructthepatienttoextendhisarmfromaflexedposition.Beforethepatientreaches90°,begintoresistthepatientmotionuntilyouhavediscoveredthemaximumresistancethepatientcanovercome(Fig.1-19).Yourresistanceshouldbeconstantandfirm,becauseajerky,pushingtypeofresistancecannotpermitanaccurateevaluation.Notethatgravityisnormallyavaluableaidinelbowextension;ifextensionseemsveryweak,youmustaccountforit,aswellasfortheweightofthearm.Ifextensionseemsweakerthangrade3,testthetricepsinagravity-freeplane.Tricepsstrengthisimportantbecauseitpermitsthepatienttosupportweightbearingonacaneorastandardcrutch(Fig.1-20).

FIGURE1-14WristdeviationwithC6andC7injuries.

FIGURE1-15Brachioradialisreflextest,C6.

FIGURE1-16AneasywaytorememberthesensorydistributionofC6.

FIGURE1-17C7:Tricepsextension,wristflexion,andfingerextension.

WristFlexorGroup:C7(MedianandUlnarNerves)1. Flexorcarpiradialis(Fig.1-12)

Mediannerve,C72. Flexorcarpiulnaris

Ulnarnerve,C8Theflexorcarpi radialis (C7) is themore importantof these twomuscles

andprovidesmostofthepowerforwristflexion.Theflexorcarpiulnaris,whichis primarily innervated by C8, provides less power but acts as an axis forflexion.Tounderstandthis,notetheulnardirectionthatnormalflexiontakes.

FIGURE1-19ATricepsbrachii.Origin:Longheadfrominfraglenoidtuberosityofscapula,lateralheadfromposteriorandlateralsurfacesofhumerus,medialheadfromlowerposteriorsurfaceofhumerus.Insertion:Upperposteriorsurfaceofolecranonanddeepfasciaofforearm.

FIGURE1-19BMuscletestofthetricepsmuscle.

FIGURE1-20Walkingwithastandardcrutchrequiresanactivetricepsmuscle.

Toprepareforthewristflexiontest,instructthepatienttomakeafist.Thefingerflexorscan,insomeinstances,actaswristflexors;fingerflexionremovesthemasfactorsduringthetest,becausethemuscleshavecontractedbeforethetest begins. Stabilize the wrist, then instruct the patient to flex a closed fist.When thewrist is in flexion, hold the patient’s closed fist and try to pull thewristoutofitsflexedposition(Fig.1-21).

FingerExtensors:C7(RadialNerve)1. Extensordigitorumcommunis(Fig.1-22)2. Extensorindicisproprius3. Extensordigitiminimi

To testextensionof thefingers,stabilize thewrist in theneutralposition.Instruct the patient to extend their metacarpophalangeal joints and flex theinterphalangeal joints at the same time. Flexion of the interphalangeal jointspreventsthesubstitutionoftheintrinsicmusclesofthehandforthelongfingerextensors.Placeyourhandon thedorsumof theextendedproximalphalangesandtrytoforcethemintoflexion(Fig.1-23).

ReflexTestingTricepsReflex:ThetricepsreflexisinnervatedbytheC7componentoftheradialnerve.

To test the reflex of the triceps muscle, rest the patient’s arm on yourforearm; the position is exactly the same as it was in the test for the bicepsreflex.Instructthepatienttorelaxhisarmcompletely.Whenyouknowthatthearmis relaxed(youcanfeel the lackof tension in the tricepsmuscle), tap thetriceps tendonas itcrosses theolecranonfossa(Fig.1-24).The triceps tendonshouldjerkslightly,amovementthatyoucaneitherfeelalongyoursupportingforearmorsee.

FIGURE1-21AFlexorcarpiradialis(left).Origin:Commonflexortendonfrommedialepicondyleofhumerus,fasciaofforearm.Insertion:Baseof2dand3dmetacarpalbones.

FIGURE1-21BMuscletestforthewristflexors.

FIGURE1-22AFingerextension—C7;fingerflex—C8.

FIGURE1-22BExtensordigitorum.Origin:Lateralepicondyleofhumerusbycommonextensortendon,intermuscularsepta.Insertion:Lateralanddorsalsurfacesofphalangesofmedialfourdigits.

FIGURE1-23Muscletestforfingerextension.

FIGURE1-24Tricepsreflextest.

SensationTesting

MiddleFinger:C7suppliessensationtothemiddlefinger.BecausemiddlefingersensationisalsooccasionallysuppliedbyC6andC8,thereisnoconclusivewaytotestC7sensation.

NeurologicLevelC8

MuscleTestFingerFlexors1. Flexordigitorumsuperficialis(Fig.1-22)

Mediannerve,C82. Flexordigitorumprofundus

Medianandulnarnerves,C83. Lumbricals

Medianandulnarnerves,C8(T1)The flexor digitorum profundus, which flexes the distal interphalangeal

joint, and the lumbricals, which flex the metacarpophalangeal joint, usuallyreceiveinnervationfromtheulnarnerveontheulnarsideofthehandandfromthemediannerveontheradialside.IfthereisaninjurytotheC8nerveroot,theentire flexordigitorumprofundusbecomesweak,with secondaryweakness inall finger flexors. If, however, there is a peripheral injury to the ulnar nerve,weakness will exist only in the ring and little fingers. The flexor digitorumsuperficialis,which flexes theproximal interphalangeal joint,hasonlymediannerveinnervationandisaffectedbyrootinjurytoC8andperipheralinjuriestothemediannerve(Fig.1-25).

To test flexionof the fingers, instruct thepatient to flexhis fingersat allthreesetsofjoints:themetacarpophalangealjoints,theproximalinterphalangealjoints,andthedistalinterphalangealjoints.Thencurlorlockyourfourfingersinto the patients (Fig. 1-26). Try to pull the fingers out of flexion. As youevaluate the results of your test, notewhich joints fail to hold flexion againstyourpull.Normally,alljointsshouldremainflexed.ToremembertheC8motorlevelmoreeasily,notethatthemuscletesthasfourofyourfingersintertwinedwithfourofthepatient’s;thesumequalseight(Fig.1-27).

SensationTestingMedialForearm(MedialAntebrachial-CutaneousNerve):C8suppliessensationtotheringandlittlefingersofthehandandthedistalhalfoftheforearm.The

ulnarsideofthelittlefingeristhepurestareaforsensationoftheulnarnerve(whichispredominantlyC8)andisthemostefficientlocationfortesting.Testtheoppositesideasameansforcomparisonandgradeyourpatient’ssensationasabsent(anesthesia),diminished(hypoesthesia),normal,orincreased(hyperesthesia)(Fig.1-28).

FIGURE1-26AFlexordigitorumsuperficialis(left).Origin:Humeralheadfromcommonflexortendonfrommedialepicondyleofhumerus,ulnarheadfromcoronoidprocessofulna,radialheadfromobliquelineofradius.Insertion:Marginsofpalmarsurfaceofmiddlephalanxofmedialfourdigits.

FIGURE1-26BLumbricals.Origin:Therearefourlumbricals,allarisingfromtendonsofflexordigitorumprofundus:1stfromradialsideoftendonforindexfinger,2dfromradialsideoftendonformiddlefinger,3dfromadjacentsidesoftendonsformiddleandringfingers,4thfromadjacentsidesoftendonsforringandlittlefingers.Insertion:Withtendonsofextensordigitorumandinterosseiintobasesofterminalphalangesofmedialfourdigits.

FIGURE1-26CMuscletestingofthefingerflexors.

NeurologicLevelT1Test T1 for its motor and sensory components, because T1, like C8, has noidentifiablereflexassociatedwithit(Fig.1-29).

MuscleTestingFingerAbduction1. Dorsal interossei (DAB)—(The initials indicate that the Dorsal interossei

ABduct.)Ulnarnerve,T1(Fig.1-30)2. Abductordigitiquinti(5finger)

Ulnarnerve,T1

FIGURE1-27AneasywaytorememberthatC8innervatesthefingerflexors.

FIGURE1-28C8sensorydistribution.

FIGURE1-29NeurologiclevelT1.

FIGURE1-30Interosseidorsales.Origin:Therearefourdorsalinterossei,eacharisingbytwoheadsfromadjacentsidesofmetacarpalbones.

NotethatallsmallmusclesofthehandareinnervatedbyT1.Totestfingerabduction, instruct the patient to abduct their extended fingers away from theaxialmidlineof thehand.Thenpincheachpairoffingers totrytoforcethemtogether:pinchtheindextothemiddle,ring,andlittlefingers;themiddletotheringandlittlefingers;andtheringtothelittlefingers(Fig.1-31).Observeanyobvious weaknesses between pairs, and test the other hand as a means ofcomparison.

Notethatpushingthelittlefingertotheringfingerteststheabductordigitiquinti.

FingerAdductionPrimaryadductor(Fig.1-30)1. Palmar Interossei (PAD)—(The initials indicate that the Palmar interossei

ADduct.)Ulnarnerve,C8,T1Totest fingeradduction,have thepatient try tokeephisextendedfingers

togetherwhileyouattempttopullthemapart.Testinpairsasfollows:theindexandmiddlefingers,themiddleandringfingers,andtheringandlittlefingers.

FIGURE1-31Muscletestforfingerabduction.

Fingeradductioncanalsobecheckedifyouplaceapieceofpaperbetweentwoofthepatient’sextendedfingersandpullitoutfrombetween.Thestrengthofhisgraspshouldbecomparedwiththatoftheoppositehand(Fig.1-32).Toremember the T1 neurologic level more easily, pull a one-dollar bill frombetweentheextendedfingersandassociatetheonedollarwithneurologiclevelT1.

SensationTestingMedialArm(MedialBrachialCutaneousNerve):T1suppliessensationtotheupperhalfofthemedialforearmandthemedialportionofthearm(Fig.1-33).

SummaryThefollowingschemeisrecommendedfortestingneurologiclevelsintheupperextremity.Intheneurologicexaminationoftheupperextremity,itispracticaltoevaluate all motor power first, then all reflexes and finally sensation. Thismethodpermitseconomyofeffortandcreatesaminimumofdisturbanceforthepatient.

Motorpowercanbetestedalmostcompletelyinthewristandhandwithminimalmotionandeffort for theexaminerandpatient.Wristextension (C6),wrist flexion and finger extension (C7), finger flexion (C8), and fingerabductionandadduction(T1)canallbeperformedinonesmoothmotion.OnlyC5mustbetestedelsewhere,withthedeltoidandbicepsmuscles(Fig.1-34).

FIGURE1-32Muscletestforfingeradduction.

FIGURE1-33T1sensorydistribution.

Reflexescanallbeobtainedinasmoothpatterniftheelbowandextremityarestabilizedinoneposition.It istheneasytomovethereflexhammertotaptheappropriatetendon—biceps(C5),brachioradialis(C6),andtriceps(C7)(Fig.1-35).

Sensationcanalsobe tested inasmoothpattern.Startproximallyon theouter portion of the extremity and move down the extremity (C5, arm; C6,forearm),thenacrossthefingers(C6-C8).Finally,moveuptheinnerborderoftheextremity(C8,forearm;T1,arm),totheaxilla(T2)(Fig.1-36).

FIGURE1-34Summaryofmuscletestingfortheupperextremity.

FIGURE1-35Summaryofreflextestingfortheupperextremity.

FIGURE1-36Summaryofsensationfortheupperextremity.

NEUROLOGICLEVELSINUPPEREXTREMITYMotor

C5—ShoulderabductionC6—WristextensionC7—WristflexionandfingerextensionC8—FingerflexionT1—Fingerabduction,adduction

SensationC5—LateralarmC6—Lateralforearm,thumb,andindexfingerC7—Middlefinger(variable)C8—Medialforearm,ring,andsmallfingerT1—Medialarm

T2—AxillaReflex

C5—BicepsC6—BrachioradialisC7—Triceps

ClinicalApplicationofNeurologicLevelsHerniatedCervicalDisksThere are eight cervical nerves and only seven cervical vertebrae; thus, eachcervical nerve leaves the spine adjacent to its corresponding vertebral bodyexceptC8, the first cervicalnerveexitsbetween theocciputandC1, the sixthbetweenC5andC6,andtheeighthbetweenC7andT1(Fig.1-37).Aherniateddisk impingesupon thenerve rootexitingabove thediskandpassing throughthe nearby neural foramen and results in the involvement of one specificneurologic level. For example, a herniated disk betweenC5 andC6 impingesupontheC6nerveroot(Fig.1-38).Whenadiskherniatesintoanerveroot,painradiatesalongthepathofthenerverootbeingirritated.

FIGURE1-37Cervicalvertebraeandnerveroots.

ThereisslightlymoremotionbetweenC5andC6thanbetweentheothercervical vertebrae (except for between the specialized articulations of theocciputandC1,andC1andC2)(Figs.1-39and1-40).Greatermotioncausesagreater potential for breakdown, and the incidence of herniated disks andosteoarthritis isgreateratC5-C6 thanatanyof theothercervicaldiskspaces.The incidenceofherniation increasesatC6-C7as thepatientgrowsolder; thereasonsforthisarenotyetknown.

Toinvolvethenerveroot, thedisksmustherniateposteriorly.Theydosofor two reasons: first, the annulus fibrosus is intact and strong anteriorly anddefectiveposteriorly;second,theanteriorlongitudinalligamentisanatomicallybroaderandstrongerthanthenarrowerposteriorlongitudinalligament.Becauseadiskusuallyherniatesunderpressure,itbreaksthroughinthedirectionofleastresistance, posteriorly. Because of the rhomboidal shape of the posteriorlongitudinal ligament, the disk also tends to herniate to one side or the other(Fig. 1-41); it is less common to have amidline herniation, because the diskwouldthenhavetopenetratethestrongestportionoftheligament.

FIGURE1-38Aherniatedcervicaldisk.

FIGURE1-39SpecializedarticulationbetweentheocciputandC1allowingfor50percentoftheflexionandextensioninthecervicalspine.

FIGURE1-40SpecializedarticulationbetweenC1andC2allowingfor50percentoftherotationinthecervicalspine.

Paininonearmortheotherissymptomaticofherniatedcervicaldisks;thepainusuallyradiatestothehandalongtheneurologicpathwaysoftheinvolvedroot,although,occasionally,thepainmaybereferredonlyasfarastheshoulder.Coughing, sneezing, or straining usually aggravates the pain and causes it toradiatethroughouttheinvolvedneurologicdistributionintheextremity.

FIGURE1-41Theanatomicbasisforposteriorcervicaldiskherniation.

Thesymptomsandsignscausedbyaherniateddiskvarydependingonthelocationoftheherniation.Iftheherniationislateral,asismostcommon,itmayimpinge directly upon the nerve root, giving classical root-level neurologicfindings.However, if thediskherniates in themidline, the symptomsmaybeevidentinthelegandarmaswell(Fig.1-42).Ifthediskprotrudesbutdoesnotherniate, pain may be referred to the midline of the back in the area of thesuperiormedialportionsofthescapulae(Fig.1-43).Lateralprotrusionmaysendpain along the spinous border of the scapula (most commonly to the superiormedial angles), with radiation of pain down the arm, but usually withoutneurologicfindings.

Occasionally, there may be inconsistent findings of neurologic levelinvolvement during the examination. Sometimes the brachial plexus, whichusuallyincludesthenerverootsC5-T1,willbeginalevelhigher(prefixed)oralevel lower (postfixed), causing variations in the segmental innervation of themuscles; the findings will reflect this inconsistency in the innervation of theupper extremity. It is also possible that suchmajor inconsistencies are due tobrachialplexusorperipheralnerveinjuries.

FIGURE1-42Patternofpainradiationwithamidlineherniatedcervicaldisk.

SpecificTestsforLocatingHerniatedCervicalDisksToestablishtheexactneurologiclevelofinvolvementsecondarytoaherniateddisk, use the neurologic evaluation technique described earlier in this chapter(Figs.1-44to1-48).

Table1-1summarizes theareasofneurologic level testing. Inaddition, itdemonstratestheclinicalapplicationofneurologicleveltestingtopathologyinthe cervical spine, especiallywith regard to the evaluation of herniated disks.Otherwaysoflocatingherniateddisksarethroughthefollowing:1. The magnetic resonance imaging (MRI), which reveals the abnormal

protrusionofaherniateddiskintothespinalcord,nerveroot,orcaudaequinaattheinvolvedlevel.

2. Myelogram,whichisatestwherecontrastdyeisinjectedintothespine,afterwhichacomputedtomographyscanisperformedtolookforproblemsinthespinalcanal, includingspinalcord,nerve roots,andother tissue.The test iscommonly reserved for patients who have previously had spine surgery orwhocannothaveanMRI(Fig.1-49).

3. The electromyogram (EMG), which accurately measures motor potentials.Twoweeksafterinjurytoanerve,abnormalspontaneouselectricaldischargesappearintherestingmuscle(fibrillationpotentialsandpositivesharpwaves).Theseareevidenceofamuscledenervation,whichcanresultfromherniateddisks, nerve root avulsions, or cord lesions. (They can alsooccur in plexusandperipheralnerve lesions.) It is important thatmuscles representingeachneurologiclevel(myotome)besampledforacompleteevaluation(seeTable1-1).

FIGURE1-43Patternofpainradiationwithalateralprotrusionofacervicaldisk.

FIGURE1-44AherniateddiskbetweenvertebraeC4andC5involvestheC5nerveroot.

GeneralTestforHerniatedCervicalDisksThe Valsalva test is a generalized test that indicates only the presence of aherniated disk. The tests of each neurologic level are more precise and canpinpointtheexactlevelofinvolvement.

ValsalvaTest:TheValsalvatestincreasestheintrathecalpressure.Ifthereisaspace-occupyinglesioninthecervicalcanal,suchasaherniateddiskoratumor,thepatientwilldeveloppaininthecervicalspinesecondarytotheincreasedpressure.Thepainmayradiatetotheneurologicdistributionoftheupperextremitythatcorrespondstothepathologicallyinvolvedneurologiclevel.

ToperformtheValsalvatest,havethepatientbeardownasifmovingthebowelswhileholdingthebreath.Thenaskthepatientifthereisanyincreaseinpaineitherinthecervicalspineor,byreflection,intheupperextremity(Fig.1-

50).TheValsalva test is a subjective test that requires that the patient answeryour questions appropriately; if the patient is either unable or unwilling toanswer,thetestisoflittlevalue.

CervicalNeckSprainversusHerniatedDiskPatientsfrequentlydevelopneckpainafterautomobileaccidentsthatcausethecervicalspinetowhipbackandforth(whiplash)or twist (Fig.1-51A,B).Theresulting injury may stretch an individual nerve root, cause a nerve root toimpingeuponanosteoarthriticspur,orproduceaherniateddisk.Patientswithneurologicinvolvementcomplainofneckpainreferredtothemedialborderofthe scapula and radiating down the arm to varying degrees, as well as ofnumbnessandmuscleweaknessintheextremity.However,suchaninjurymaysimplystretchtheposteriororanteriorneckmuscles,causingasimilarneckpainwithradiationtotheshoulderandmedialborderofthescapula.

FIGURE1-45AherniateddiskbetweenvertebraeC5andC6

involvestheC6nerveroot.Thisisthemostcommonlevelofdiskherniationinthecervicalspine.

Differentiation between generalized soft-tissue injury without neurologicinvolvementandinjurywithneurologicinvolvementcanbemadebytestingtheintegrity of theneurologic levels innervating theupper extremities.With eachpatient visit, neurologic testing must be repeated, because an originallyquiescent lesionmay later clinicallymanifest itself. Note that the converse isalso true: patients who are hospitalized for treatment of neurologic problemsmay show improved muscle strength, return of a reflex, or return of normalsensationtotheinvolveddermatome.

Manypatientscontinue tocomplainofcervicalpainsixmonths toayearafterinjurywithoutevidenceofeitherneurologicorobjectiveMRIfindingsofpathology.Thepractitionershouldhavetheconfidence,despitepatientpressure,to continue conservative (nonoperative) therapy, knowing that thepatientmayhave a permanent soft-tissue injury not involving the anterior primary nerverootsortheintervertebralcervicaldisks.

FIGURE1-46AherniateddiskbetweenvertebraeC6andC7involvestheC7nerveroot.

TheUncinateProcessesandOsteoarthritisThe uncinate processes are two ridges of bone that originate on the superiorlateral surface of the cervical vertebrae. They help to stabilize the individualvertebra and participate in the formation of the neural foramen (Fig. 1-52).Enlargements or osteoarthritis involving the uncinate process may encroachupontheneuralforamenanddirectlycompresstheexitingnerverootorlimittheamountofroominwhichitcanmove(Fig.1-53).

Theneuralforamenandportionoftheuncinateprocessencroachinguponitcanbeseenonanx-ray(Fig.1-54).Note that thenerverootsemergeata45°anglefromthecordandvertebralbody,thesameanglethatexistsbetweentheneuralforamenandthevertebralbody.Anosteophytefromtheuncinateprocesshas little clinical significance unless it is accompanied by symptoms.Clinicalproblems may arise after an automobile accident, when a patient with anarrowedneuralforamenmayplaceexcessivestrainonthenerverootlyinginitbecause of the extreme extension/flexion of the head and neck and thesubsequent reactive edemaof the nerve root.Note that the narrowed foramenfrequentlyhasthex-rayappearanceofafigure8,aconfigurationthatdoesnotallowroomfortheposttraumaticswellingofthenerveandresultsinpain.Painandneurologicfindingsarenaturallyfoundintheinvolvedneuraldistributionintheupperextremity.Forexample,traumaaffectingtheC6nerverootmayresultin decreased sensation to the lateral forearm, muscle weakness to the wristextensors, and an absent brachioradialis reflex (Fig. 1-40). It is also possible,however,thattheonlysymptomreferredispaintothesuperiormedialangleandmedialborderofthescapula.

FIGURE1-47AherniateddiskbetweenvertebraeC7andT1involvestheC8nerveroot.

Where there ismoremotion, there isagreaterchanceofbreakdown,anduncinateprocessenlargementsecondarytoosteoarthritisismostoftenfoundattheC5-C6bonylevel.

SpurlingTestThe cervical spine compression test determines whether the patient’s pain isincreasedwhenthecervicalspine iscompressed.Paincausedbynarrowingofthe neural foramen, pressure on the facet joints, or muscle spasm may beincreasedbycompression.Thecompression testmayalso faithfully reproducepainreferreddowntheupperextremityfromthecervicalspine; indoingso, itmayassistinlocatingtheneurologiclevelofexistingpathology.

FIGURE1-48AherniateddiskbetweenvertebraeT1andT2involvestheT1nerveroot.Aherniateddiskinthisareaisunusual.

To perform the compression test, have the patient turn their head to theaffectedsideandslightlyextendtheirhead.Pressonthetopofthepatient’sheadwhile thepatient iseithersittingor lyingdown;discoverwhether there isanycorrespondingincreaseinpaineitherinthecervicalspineordowntheextremity.Note the exact distribution of this pain andwhether it follows any previouslydescribeddermatome(Fig.1-55).

NerveRootAvulsionsCervical nerve roots are frequently avulsed from the cord during motorcycleaccidents.Whenarideristhrownfromhiscycle,hisheadandneckareforcedlaterally,andhisshoulder isdepressedby the impactwith theground,causingthecervicalnerverootstostretchandfinallyavulse(Fig.1-56).TheC5andC6

nerverootsaretherootsmostcommonlyavulsed.Physical examination shows the obvious results: with the loss of the C5

root, there is totalmotor paralysis along theC5myotome and sensory deficitalong theC5dermatome.Thedeltoidmuscle isparalyzed,sensationalong theupperlateralportionofthearmishypestheticoranesthetic,andthebicepsreflex(C5-C6)isdiminishedorabsent.TheMRIshowsanavulsion,theoriginoftheC5nerverootbetweentheC4andC5vertebrae.Suchalesionisnotamenabletosurgicalrepair.Theinjuryispermanent;norecoveryistobeexpected.

TABLE1-1UNDERSTANDINGHERNIATEDDISKSANDOSTEOARTHRITISOFTHECERVICALSPINE

ROOTDISKMUSCLESREFLEX SENSATION EMG MYELOGRAMUNCINATEPROCESS

C5 C4-C5

DeltoidBiceps

Biceps LateralarmAxillarynerve

Fibrillationorsharpwavesindeltoid,biceps†

BulgeinspinalcordC4-C5

C6* C5-C6

BicepsWristextensors

Brachioradialis LateralforearmMusculocutaneousnerve

Fibrillationorsharpwavesinbiceps‡

C7 C6-C7

TricepsWristflexorsFingerextensors

Triceps Middlefinger Fibrillationorsharpwavesintriceps§

C8 C7-T1

HandintrinsicsFingerflexors

MedialforearmMedialantebrachial-cutaneousnerve

Fibrillationorsharpwavesinintrinsichandmuscles|

BulgeinspinalcordC7-T1

T1 T1-T2

Handintrinsics

MedialarmMedialbrachial-cutaneousnerve

Fibrillationorsharpwavesinhandmuscles

*Mostcommonlevelofherniation.†Deltoid,rhomboid,supraspinatus,andinfraspinatusmuscles.‡Extensorcarpiradialislongusandbrevis.§Triceps,flexorcarpiradialis,extensordigitorumlongus.|Flexordigitorummuscles.

FIGURE1-49MRI:herniateddiskatC5-C6.

FIGURE1-50TheValsalvatest.

FIGURE1-51A,BWhiplashinjurytothecervicalspine.

FIGURE1-52Theanatomyofacervicalvertebra.

FIGURE1-53Osteoarthritisoftheuncinateprocess.

FIGURE1-54Narrowedneuralforamensecondarytoosteoarthritisoftheuncinateprocess,C3-C4.

FIGURE1-55Compressiontest.(Hoppenfeld,S.:PhysicalExaminationoftheSpineandExtremities.Norwalk,CT:Appleton-Century-Crofts,1976.)

AlthoughC5andC6arethemostcommonlyavulsedroots,theC8andT1may also be avulsed. If the cyclist strikes the ground with his shoulderhyperabducted, the lowest roots of the brachial plexus are usually the onesinjured,whereastheC5andC6nerverootsremainintact.

FIGURE1-56AvulsionoftheC5nerverootfollowingamotorcycleaccident.

EvaluationofNerveRootLesionsInvolvingtheTrunkandLowerExtremity

Manifestationsofpathologyinvolvingthespinalcordandcaudaequina,suchasherniateddisks,tumors,oravulsednerveroots,arefrequentlyfoundinthelowerextremity. Understanding the clinical relationship between various muscles,reflexes, and sensory areas in the lower extremity and their neurologic levels(cord levels) is particularly helpful in detecting and locating spinal problemswithgreateraccuracyandease.

Tomaketherelationshipbetweenthespineandthelowerextremityclear,the neurologic examination of the lumbar spine is divided into tests of eachneurologic levelanditsdermatomesandmyotomes.Thus,foreachneurologiclevelofthelowerspinalcord,themuscles,reflexes,andthesensoryareasthatmostclearlyreceiveinnervationfromitistested.

TestingofIndividualNerveRoots,T2-S4NeurologicLevelsT2-T12

MuscleTestingIntercostals:Theintercostalmusclesaresegmentallyinnervatedandaredifficulttoevaluateindividually.

RectusAbdominis:TherectusabdominismusclesaresegmentallyinnervatedbytheprimaryanteriordivisionsofT5-T12(L1),withtheumbilicusthedividingpointbetweenT10andT11.

Beevor’ssign(Fig.2-1)teststheintegrityofthesegmentalinnervationoftherectusabdominismuscles.Askthepatienttodoaquartersit-up.Whilethepatientisdoingthis,observetheumbilicus.Normally,itshouldnotmoveatallwhen the maneuver is performed. If, however, the umbilicus is drawn up ordown or to one side or the other, be alerted to possible asymmetricalinvolvement of the anterior abdominalmuscles. Lesions of the spinal cord orrootsbetweenT10andT12willcauseweaknessofthelowerpartofthemuscle,andthusapositiveBeevor’ssidewiththeumbilicusmovingupwardduringthequartersit-up.

FIGURE2-1Beevor’ssign.

SensoryTestingSensoryareasforeachnerverootareshowninFigure4-1.ThesensoryareaforT4crossesthenippleline,T7thexiphoidprocess,T10theumbilicus,andT12thegroin.Thereissufficientoverlapoftheseareasfornoanesthesiatoexistifonlyonenerverootisinvolved.However,hypoesthesiaisprobablypresent.

NeurologicLevelsT12-L3

MuscleTestingThere is no specific muscle test for each root. The muscles that are usuallytested are the iliopsoas (T12-L3), the quadriceps (L2-L4), and the adductorgroup(L2-L4).

Iliopsoas:(Branchesfrom[T12],L1-L3):Theiliopsoasmuscleisthemainflexorofthehip(Fig.2-2).Totestit,instructthepatienttositontheedgeoftheexaminingtablewiththelegsdangling.Stabilizethepelvisbyplacingyourhandoverthepatient’siliaccrestandhavethepatientactivelyraisetheirthighoffthetable.Nowplaceyourotherhandoverthedistalfemoralportionofthekneeandaskthepatienttoraisethethighfurtherasyouresist(Fig.2-3).Determinethemaximumresistancethepatientcanovercome.Thenrepeatthetestfortheoppositeiliopsoasmuscleandcomparemusclestrengths.Becausetheiliopsoasreceivesinnervationfromseverallevels,amusclethatisonlyslightlyweakerthanitscounterpartmayindicateneurologicproblems.

FIGURE2-2A(T12),L1-L3—hipflexion.

FIGURE2-2BIliopsoas.Origin:Anteriorsurfaceofthebodiesofalllumbarvertebraeandtheirtransverseprocessesandcorrespondingintervertebraldisks.Uppertwo-thirdsoftheiliacfossa.Insertion:Lessertrochanteroffemur.

FIGURE2-3Muscletestfortheiliopsoas.

In addition to possible neurologic pathology, the iliopsoas may becomeweak as a result of an abscess within its substance; the patient may thencomplainofpainduringmuscletesting.Themusclemayalsobecomeweakasaresultofkneeorhipsurgery.

Quadriceps:L2-L4(FemoralNerve):Totestthequadricepsfunctionally,instructthepatienttostandfromasquattingposition(Fig.2-4).Notecarefullywhetherthepatientstandsstraight,withthekneesinfullextension,orwhetheronelegisusedmorethantheother.Thearcofmotionfromflexiontoextensionshouldbesmooth.Occasionally,thepatientmaybeabletoextendthekneesmoothlyonlyuntilthelast10°,finishingthemotionhaltinglyandwithgreat

effort.Thisfalteringinthelast10°ofextensioniscalledextensionlag;itoccursbecausethelast10°to15°ofkneeextensionrequiresatleast50percentmoremusclepowerthantherest(accordingtoJacquelinePerry).Extensionlagisfrequentlyseeninassociationwithquadricepsweakness.Sometimes,thepatientmaybeunabletoextendhiskneethroughthelast10°witheventhegreatesteffort(Fig.2-5).

FIGURE2-4AL2-L4—kneeextension.

FIGURE2-4BRectusfemoris.Origin:Rectusfemorisisa“two-joint”musclethathastwoheadsoforigin.Straighthead:fromanteriorinferioriliacspine.Reflectedhead:fromgroovejustabovebrimofacetabulum.Insertion:Upperborderofpatella,andthenintothetibialtubercleviatheinfrapatellartendon.FIGURE2-4CVastusintermedius.Origin:Uppertwo-thirdsofanteriorandlateralsurfaceoffemur.Insertion:Upperborderofthepatellawiththerectusfemoristendonandthenviatheinfrapatellartendonintothetibialtubercle.Vastuslateralis.Origin:Capsuleofhipjoint,intertrochantericline,glutealtuberosity,lineaaspera.Insertion:Proximalandlateralborderofpatella,andintotibialtubercleviatheinfrapatellartendon.

Vastusmedialis.Origin:Lowerhalfofintertrochantericline,lineaaspera,medialsupracondylarline,medialintermuscularseptum,tendonofadductormagnus.Insertion:Medialborderofpatellaandintotibialtubercleviatheinfrapatellartendon.

FIGURE2-5Extensionlag.(Hoppenfeld,S.:PhysicalExaminationoftheSpineandExtremities.Norwalk,CT:Appleton-Century-Crofts,1976.)

Totestthequadricepsmanually,stabilizethethighbyplacingonehandjustabove the knee. Instruct the patient to extendhis knee as youoffer resistancejust above the ankle joint. Palpate the quadriceps during the test with yourstabilizinghand(Fig.2-6).Notethatthequadricepsweaknesscanalsobeduetoareflexdecreaseinmusclestrengthfollowingkneesurgeryortotearswithinthesubstanceofthemuscleitself.

FIGURE2-6Muscletestforthequadriceps.

HipAdductorGroup:L2-L4(ObturatorNerve):Likethequadriceps,thehipadductorscanbetestedasamassivegrouping(Fig.2-7).Havethepatientliesupineorontheirsideandinstructthepatienttoabductthelegs.Placeyourhandonthemedialsidesofbothkneesandhavethepatientadducttheirlegsagainstyourresistance(Fig.2-8).Determinethemaximumresistancetheycanovercome.

ReflexesAlthoughthepatellartendonreflexissuppliedbyL2-L4,itispredominantlyL4andwillbetestedassuch.

SensoryTestingNerves fromL1 toL3 provide sensation over the general area of the anterior

thigh between the inguinal ligament and the knee. The L1 dermatome is anobliquebandontheupperanteriorportionofthethigh,immediatelybelowtheinguinalligament.TheL3dermatomeisanobliquebandontheanteriorthigh,immediatelyabovethekneecap.Betweenthesetwobands,ontheanterioraspectofthemidthigh,liestheL2dermatome(Fig.2-9).

FIGURE2-7AL2-L4—hipadduction.

FIGURE2-7BAdductorbrevis(center).Origin:Outersurfaceofinferiorramusofpubis.Insertion:Lineextendingfromlessertrochantertolineaasperaandupperpartoflineaaspera.Adductorlongus(left).Origin:Anteriorsurfaceofthepubisintheanglebetweencrestandpubicsymphysis.Insertion:Lineaaspera,middlehalfofmediallip.Adductormagnus(right).Origin:Ischialtuberosity,inferiorramiofischiumandpubis.Insertion:Lineextendingfromgreatertrochantertolineaaspera.Theentirelengthoflineaaspera,medialsupracondylarline,andadductortubercleofthefemur.

FIGURE2-8Muscletestforhipadductors.

Sensory testing, with its bands of individual dermatomes, is a moreaccuratewayofevaluatingneurologiclevelsT12-L3thanmotortesting,whichlacksindividualrepresentativemuscles.Therearealsonorepresentativereflexesfor these levels,makingitevenmoredifficult todiagnoseanexactneurologiclevel.NeurologiclevelsL4,L5,andS1arerepresentedbyindividualmuscles,dermatomes,andreflexes,andareeasiertodiagnose.

NeurologicLevelL4

MuscleTestingTibialis Anterior: L4 (Deep Peroneal Nerve): The tibialis anterior muscle ispredominantly innervated by the L4 segmental level; it also receives L5

innervation(Figs.2-10and2-11).Totestthemuscleinfunction,askthepatienttowalkonhis heelswithhis feet inverted.The tendonof the tibialis anteriormusclebecomesvisibleasitcrossestheanteromedialportionoftheanklejointandisquiteprominentasitproceedsdistallytowarditsinsertion.Patientswithweaktibialisanteriormusclesareunabletoperformthisfunctionaldorsiflexion-inversiontest;theymayalsoexhibit“dropfoot,”orsteppagegait.

FIGURE2-9Dermatomesofthelowerextremity.

Totestthetibialisanteriormanually,instructthepatienttositontheedge

of the examining table. Support his lower leg, and place your thumb in apositionthatmakeshimdorsiflexandinverthisfoottoreachit.Trytoforcethefootintoplantarflexionandeversionbypushingagainst theheadandshaftofthefirstmetatarsal;palpatethetibialisanteriormuscleasyoutestit(Fig.2-12).

FIGURE2-10NeurologiclevelL4.

FIGURE2-11AL4,L5—footinversion.FIGURE2-11BTibialisanterior.Origin:Lateralcondyleoftibia,uppertwo-thirdsoftheanterolateralsurfaceoftibia,interosseusmembrane.Insertion:Medialandplantarsurfacesofmedialcuneiformbone,baseof1stmetatarsalbone.

FIGURE2-12Muscletestforthetibialisanterior.

ReflexTestingPatellar Tendon Reflex: The patellar tendon reflex is a deep tendon reflex,mediatedthroughnervesemanatingfromtheL2-L4nerveroots(predominantlyfrom L4). For clinical application, the patellar tendon reflex should beconsideredanL4reflex;however,becauseitreceivesinnervationfromL2andL3 as well as from L4, the reflex will still be present, although significantlyweakened,eveniftheL4nerverootiscompletelysevered.Thereflexisalmostnever totallyabsent.However, inprimarymuscle,nerve root,or anteriorhorncelldisease,thereflexcanbetotallyabsent.

FIGURE2-13Patellartendonreflex.

Totest thepatellar tendonreflex,ask thepatient tositon theedgeof theexaminingtablewiththelegsdangling.(Thepatientmayalsositonachairwithonelegcrossedoverhiskneeor,ifthepatientisinbed,withthekneesupportedin a few degrees of flexion) (Fig. 2-13). In these positions, the infrapatellartendonisstretchedandprimed.Palpatethesofttissuedepressiononeithersideof the tendonto locate itaccurately,andattempt toelicit thereflexbytappingthetendonat thelevelof thekneejointwithashort,smartwristaction.If thereflexisdifficulttoobtain,reinforceitbyhavingthepatientclasphishandsandattempttopullthemapartasyoutapthetendon.ThisisknownastheJendrassikmaneuver.Itpreventsthepatientfromconsciouslyinhibitingorinfluencinghisorherresponsetoreflextesting.Repeattheprocedureontheoppositeleg,andgrade the reflex as normal, increased, decreased, or absent. To remember theneurologiclevelofthereflex,associatethefactthatfourmusclesconstitutethe

quadricepsmusclewiththeL4ofthepatellartendonreflex(Fig.2-14).The reflexmaybeaffectedbyproblemsother thanneurologicpathology.

For example, if the quadriceps has been traumatized, if the patient hasundergonerecentsurgerytotheknee,orifthereiskneejointeffusion,thereflexmaybeabsentordiminished.

SensoryTestingTheL4dermatomecoversthemedialsideofthelegandextendstothemedialsideofthefoot.ThekneejointisthedividinglinebetweentheL3dermatomeaboveandtheL4dermatomebelow.Ontheleg,thesharpcrestofthetibiaisthedividing line between the L4 dermatome on the medial side and the L5dermatomeonthelateralside(Fig.2-15).

FIGURE2-14AneasywaytorememberthatthepatellartendonreflexisinnervatedbyL4istoassociatethefourquadricepsmuscleswiththeneurologiclevelL4.

FIGURE2-15L4andL5sensorydermatome.

NeurologicLevelL5

MuscleTesting(Figs.2-16to2-18)1. Extensorhallucislongus2. Extensordigitorumlongusandbrevis3. Gluteusmedius

FIGURE2-16NeurologiclevelL5.

ExtensorHallucisLongus:L5(DeepBranchofthePeronealNerve):Thetendonoftheextensorhallucislonguspassesinfrontoftheanklejointlateraltothe tibialis anterior, which is predominately innervated by L4. Test itfunctionally by having the patient walk on his heels, with his feet neitherinverted nor everted. The tendon should stand out clearly on the way to itsinsertionat theproximalendof thedistalphalanxof thegreat toe.To test theextensorhallucislongusmanually,havethepatientsitontheedgeofthetable.Support thefootwithonehandaround thecalcaneusandplaceyour thumbinsuchapositionthatthepatientmustdorsiflexhisgreattoetoreachit.Opposethisdorsiflexionbyplacingyourthumbonthenailbedofthegreattoeandyourfingersontheballof thefoot; thenpulldownonthetoe(Fig.2-19A). Ifyourthumbcrossestheinterphalangealjoint,youwillbetestingtheextensorhallucis

brevisaswellasthelongus;makecertainthatyouapplyresistancedistaltotheinterphalangeal joint so that you are testingonly the extensor hallucis longus.Notethatafractureofthegreattoeorotherrecenttraumawillproduceapparentmuscleweaknessintheextensorhallucislongus.

ExtensorDigitorumLongusandBrevis:L5(DeepPeronealNerve):Testtheextensordigitorumlongusinfunctionbyinstructingthepatienttowalkonhisheels,ashedidfortheextensorhallucislongus.Thetendonoftheextensordigitorumlongusshouldstandoutonthedorsumofthefoot,crossinginfrontoftheanklemortiseandfanningouttoinsertbyslipsintothedorsalsurfacesofthemiddleanddistalphalangesofthelateralfourtoes.

Forthemanualtest,thepatientmayremainseatedontheedgeofthetable.Secure the anklewith one hand around the calcaneus and place the thumbofyourfreehandinsuchapositionthathemustextendhistoestoreachit.Opposethismotionbypressingonthedorsumofthetoesandattemptingtobendthemplantarward(Fig.2-19B).Theyshouldbevirtuallyunyielding.

FIGURE2-17L4,L5—footdorsiflexion(ankleextension).

FIGURE2-18AExtensorhallucislongus.Origin:Middlehalfofanteriorsurfaceoffibula,adjacentinterosseousmembrane.Insertion:Dorsalsurfaceofbaseofdistalphalanxofgreattoe.FIGURE2-18BExtensordigitorumlongus.Origin:Upperthree-fourthsofanteriorsurfaceoffibula,interosseousmembrane.Insertion:Dorsalsurfaceofmiddleanddistalphalangesoflateralfourtoes.FIGURE2-18CExtensordigitorumbrevis.Origin:Forepartofupperandlateralsurfaceofcalcaneus,sinustarsi.Insertion:Firsttendonintodorsalsurfaceofbaseofproximal

phalanxofgreattoe,remainingthreetendonsintolateralsidesoftendonsofextensordigitorumlongus.

FIGURE2-19AMuscletestoftheextensorhallucislongusmuscle.

FIGURE2-19BMuscletestfortoeextensors.

FIGURE2-19CAneasywaytorememberthatthetoeextensorsareinnervatedbyneurologiclevelL5.

GluteusMedius:L5(SuperiorGlutealNerve):Totestthegluteusmedius,havethepatientlieonhisside(Fig.2-20).Stabilizethepatient’spelviswithonehandandinstructthepatienttoabducttheleg.Allowthelegtoabductfullybeforeyouresistbypushingagainstthelateralthighatthelevelofthekneejoint

(Fig.2-21).Topreventthemusclesubstitutionthatmaytakeplaceifthehipisallowedtoflex,makesureitremainsinaneutralpositionthroughoutthetest.

ReflexTestingThereisnoeasilyelicitedreflexsuppliedbytheL5neurologiclevel.Althoughthe tibialis posterior muscle provides an L5 reflex, it is difficult to elicitroutinely. If, after you have performed sensory and motor tests, you are notcertain of the integrity of the L5 level, you should try to elicit the tibialisposterior reflex by holding the forefoot in a few degrees of eversion anddorsiflexion, andby tapping the tendonof the tibialis posteriormuscle on themedial side of the foot just before it inserts into the navicular tuberosity.Normally,youshouldelicitaslightplantarinversionresponse.

SensoryTestingTheL5dermatomecoversthelateralleganddorsumofthefoot.ThecrestofthetibiadividesL5 fromL4.Tomake thedistinctionbetweenL4andL5clearer,palpatethecrestofthetibiafromthekneedistallyasitanglestowardthemedialmalleolus. All that is lateral to the crest, including the dorsum of the foot,receivessensoryinnervationfromL5(seeFig.2-15).

NeurologicLevelS1

MuscleTesting1. Peroneuslongusandbrevis2. Gastrocnemius-soleusmuscles3. Gluteusmaximus

PeroneusLongusandBrevis:S1(SuperficialPeronealNerve):Theperoneimaybetestedtogetherinfunction(Figs.2-22and2-23).Becausetheyareevertorsoftheankleandfoot,askthepatienttowalkonthemedialbordersofhisfeet.Theperoneitendonsshouldbecomeprominentjustbeforetheyturnaroundthelateralmalleolus,passoneithersideoftheperonealtubercle(thebrevisabove,thelongusbelow),andruntotheirrespectiveinsertions.

FIGURE2-20L4,L5,S1—hipabduction.

FIGURE2-21AGluteusmedius.Origin:Outersurfaceofiliumbetweeniliaccrestandposteriorgluteallineabovetotheanteriorgluteallinebelow,aswellastheglutealaponeurosis.Insertion:Lateralsurfaceofgreatertrochanter.

FIGURE2-21BMuscletestforthegluteusmediusmuscle.

FIGURE2-22NeurologiclevelS1.

Totesttheperoneimusclesmanually,havethepatientsitontheedgeofthetable.Securetheanklebystabilizingthecalcaneusandplaceyourotherhandinaposition that forceshim toplantarflexandeverthis foot to reach itwithhissmalltoe.Opposethisplantarflexionandeversionbypushingagainsttheheadand shaft of the 5thmetatarsal bonewith the palm of your hand (Fig. 2-24);avoidapplyingpressuretothetoes,becausetheymaymove.

FIGURE2-23S1—footeversion.

FIGURE2-24APeroneuslongus.Origin:Headandproximaltwo-thirdsoflateralsurfaceoffibula.Insertion:Lateralsideofmedialcuneiformbone,baseof1stmetatarsalbone.Peroneusbrevis.Origin:Distaltwo-thirdsoflateralsurfaceoffibula,adjacentintermuscularsepta.Insertion:Styloidprocessofbaseof5thmetatarsalbone.FIGURE2-24BMuscletestfortheperoneimuscles.

Gastrocnemius-SoleusMuscles:S1,S2(TibialNerve):Becausethegastrocnemius-soleusgroupisfarstrongerthanthecombinedmusclesofyour

armandforearm,itisdifficulttodetectsmallamountsofexistingweakness;thegroupisthusapoorchoiceformanualmuscletestingandshouldbeobservedinfunction(Fig.2-25).Askthepatienttowalkonhistoes;thepatientwillbeunabletodosoifthereisgrossmuscleweakness.Ifthetestisnormal,instructhimtojumpupanddownontheballsofhisfeet,oneatatime,forcingthecalfmusclestosupportalmosttwo-and-a-halftimesthebody’sweight.Ifthepatientlandsflat-footedorisotherwiseincapableofperformingthistest,thereisweaknessinthecalfmuscle(Fig.2-26).Obviously,elderlypeopleorpatientswithbackpaincannotbeexpectedtoperformthisportionofthefunctionaltest.Askthesepatientstostandononelegandriseupontheirtoesfivetimesinsuccession.Inabilitytocompletethistestindicatescalfmuscleweakness.

FIGURE2-25L5,S1,S2—footplantarflexion(ankleflexion).

FIGURE2-26AGastrocnemius.Origin:Medialhead:frommedialcondyleandadjacentpartoffemur.Lateralhead:fromlateralcondyleandadjacentpartoffemur.Insertion:Intoposteriorsurfaceofcalcaneusbycalcanealtendon(Achillestendon).FIGURE2-26BSoleus.Origin:Posteriorsurfaceofheadandupperthirdofthefibula,poplitealandmiddlethirdofmedialborderoftibia,tendinousarchbetweentibiaandfibula.Insertion:Intoposteriorsurfacecalcaneusbycalcanealtendon.FIGURE2-26CMuscletestforthegastrocnemius-soleusmusclegroup.

GluteusMaximus:S1(InferiorGlutealNerve):Totestthegluteusmaximusfunctionally,havethepatientstandfromasittingpositionwithoutusinghishands(Fig.2-27).Totestitmoreaccuratelyforstrength,askhimtolieproneontheexaminingtablewithhishipsflexedovertheedgeandhislegsdangling.Havethepatientbendtheirkneetorelaxthehamstringmusclessothattheycannotassistthegluteusmaximusinhipextension.Placeyourforearmoverhisiliaccresttostabilizethepelvis,leavingyourhandfreetopalpatethegluteusmaximusmuscle.Thenaskhimtoextendhiship.Offerresistancetohipextensionbypushingdownontheposterioraspectofhisthighjustabovethekneejoint;asyouperformthetest,palpatethegluteusmaximusmusclefortone

(Fig.2-28).

ReflexTestingAchilles Tendon Reflex: The Achilles tendon reflex is a deep tendon reflex,mediated through the triceps surae. It is supplied predominantly by nervesemanating from the S1 cord level. If the S1 root is cut, the Achilles tendonreflexwillbevirtuallyabsent.

TotesttheAchillestendonreflex,askthepatienttositontheedgeoftheexamining table with the legs dangling. Put the tendon into slight stretch bygently dorsiflexing the foot. Place your thumb and fingers into the soft tissuedepressionsoneithersidetolocatetheAchillestendonaccurately,andstrikeitwiththeflatendofaneurologichammertoinduceasudden,involuntaryplantarflexionofthefoot(Fig.2-29).Itmaybehelpfultoreinforcethereflexbyhavingthepatientclasphishandsandtrytopullthemapart(orpushthemtogether)justasthetendonisbeingstruck.ToremembertheS1reflexmoreeasily,associate“AchilleS’1weakspot”withthereflex(Fig.2-30).

Therearevariousalternatemethodsof testing theAchilles tendon reflex,someofwhicharedescribedhere.Choosetheappropriatemethod,dependingontheconditionoftheparticularpatientyouareexamining.

If the patient is bedridden, cross one leg over the opposite knee so thatmovement of the ankle joint is unhindered. Prime the tendon by slightlydorsiflexingthefootwithonehandontheballofthefootandstrikethetendon.If thepatient is lyingprone inbed,ask thepatient toflex theknee to90°andprimethetendonbyslightlydorsiflexingthefootbeforeperformingthetest.Ifthe patients ankle joint is swollen, or if it is prohibitively painful to tap theAchillestendondirectly,havethepatientliepronewiththeankleovertheedgeofthebedorexaminingtable.Presstheforepartofyourfingersagainsttheballofthefoottodorsiflexitandstrikeyourfingerswiththeneurologichammer.Apositive reflex is present if the gastrocnemius muscle contracts and the footplantar flexes slightly.You should be able to detect thismotion through yourhand.

FIGURE2-27S1—hipextension.

FIGURE2-28AGluteusmaximus.Origin:Posteriorgluteallineandlaterallipofiliaccrest,posteriorsurfaceofsacrumandcoccyx.

Insertion:Iliotibialbandoffascialata,glutealtuberosityoffemur.

FIGURE2-28BMuscletestforthegluteusmaximus.

FIGURE2-28CS1dermatome.

FIGURE2-29TestofthetendonofAchillesreflex.

SensoryTestingTheS1dermatomecoversthelateralsideandaportionoftheplantarsurfaceofthefoot(Fig.2-28C).

NeurologicLevelsS2-S4Nerves emanating from the S2 and S3 neurologic levels supply the intrinsicmusclesofthefoot.Althoughthereisnoefficientwaytoisolatethesemusclesfor testing, you should inspect the toes for clawing, possibly caused bydenervation of the intrinsics. S2-S4 are also the principalmotor supply to thebladder,andneurologicproblemsthataffectthefootmayaffectitaswell.

ReflexTestingNote that there is no deep reflex supplied by S2-S4. There is, however, asuperficial anal reflex. To test it, touch the perianal skin; the anal sphinctermuscle(S2-S4)shouldcontract(wink)inresponse.

FIGURE2-30AneasywaytorememberthatthetendonofAchillesreflexisanS1reflex.

SensoryTestingThe dermatomes around the anus are arranged in three concentric rings,

receiving innervation from S2 (outermost ring), S3 (middle ring), and S4-S5(innermostring)(Fig.2-31).

SummaryThefollowingisasuggestedclinicalschemeformostneurologicleveltestinginthe lower extremity. It is practical to evaluate all motor power first, then allsensation,andfinallyallreflexes.

Mostmuscle testing of the involved lower extremity can be performedwithaminimumofeffortandmotionforexaminerandpatientifitisgenerallyconfined to the foot.Muscle testacross the foot fromthemedial to the lateralside;thetibialisanterioronthemedialsideofthefootisinnervatedbyL4,theextensor digitorum longus and brevis on the top of the foot by L5, and theperoneionthelateralsideofthefootbyS1.

FIGURE2-31SensorydermatomesS2-S5.

Sensation can also be tested in a smooth, continuous pattern across thedorsumofthefootfrommedialtolateral.ThemedialborderofthefootreceivesinnervationfromL4, the topof thefootfromL5,and the lateralborderof thefoot from S1 (Fig. 2-32). It is practical to test sensation in each extremitysimultaneouslytoobtaininstantcomparison.Theskinoveramuscleisusually

innervatedbythesameneurologiclevelasthemuscleitcovers.

FIGURE2-32Thesensorydermatomes(A)and(B)apracticalmethodoftestingsensationacrossthedorsumofthefoot.

Reflexes can be tested smoothly as well. With the patient seated, theappropriate tendons—infrapatellar tendon, L4; tendon of Achilles, S1—areeasilytested.

NEUROLOGICLEVELSINUPPEREXTREMITYMotor

L3—Quadriceps(L2-L4)L4—TibialisanteriorL5—ToeextensorsS1—Peronei

SensationT12—LowerabdomenjustproximaltoinguinalligamentL1—UpperthighjustdistaltoinguinalligamentL2—MidthighL3—LowerthighL4—Medialleg—medialsideoffootL5—Lateralleg—dorsumoffootS1—Lateralsideoffoot

S2—Longitudinalstrip,posteriorthighReflex

L4—PatellarL5—Tibialisposterior(difficulttoobtain)S1—Achillestendon

ClinicalApplicationofNeurologicLevelsHerniatedLumbarDisksLumbar disks, like cervical disks, usually herniate posteriorly rather thananteriorlyand toone side rather than in themidline; theanatomic reasons foreach type of herniation are the same (see page 25), and the disk usuallyimpinges only uponone of the twonerve roots at each level (Fig.2-33). Thepatientusuallycomplainsofpainradiatingtoonelegortheother,andrarelyofpainradiatingtobothlegsatthesametime.

Note that there is a special relationship between the nerve roots of thecaudaequinaandthediskspace.Beforeitexitsthroughtheneuralforamen,thenerverootturnsatapproximatelya45°anglearoundthepedicleofitsvertebra.Becausethepedicleissituatedintheupperthirdofthevertebralbody,thenerveroot,which is relatively tethered to it,nevercrosses thedisk spacebelowandthusisusuallynotinvolvedinanyherniationsofthediskwithinthatspace(Fig.2-34).Anerverootiscommonlyinvolvedonlyinherniationsofthedisklocatedabove its point of exit.For example, theL5nerve root crosses thedisk spacebetweenL4andL5, thenturnsaroundthepedicleofL5,andleavesthespinalcanalviatheneuralforamenbeforeitreachestheL5-S1diskspace.Itmaybeaffected by an L4-L5 herniation, but not typically by one between L5 andS1(Fig. 2-35).Thus, a patient whose symptoms are manifested along the L5distributionhasapotentialherniationinthediskspaceabovetheL5vertebra.

FIGURE2-33Theanatomicbasisforposteriorlumbardiskherniation.

TheL4-L5andL5-S1articulationshavethegreatestmotioninthelumbarspine. Greater motion causes an increased potential for breakdown, and theincidence of herniated disks is greater at L4-L5 and L5-S1 than at any otherlumbardiskspaceintheentirespine.Ninetypercentoflumbardiskherniationsoccuratthetwolevels.

FIGURE2-34Theanatomicbasisfornerverootimpingementbyaherniateddisk.

Table 2-1 delineates the applicable tests for the most clinically relevantneurologiclevels.Itappliesmostcriticallytoproblemsofherniateddisks(Figs.2-36to2-39).

Although this table reflects precise neurologic levels, the clinical picturemaynotbeasclear.Thereasonsfordiscrepanciesarenumerous.Forexample,anerverootmayoccasionallycarryelementsofadjacentnerveroots.Thus,theL4rootmaycontaincomponentsofL3orL5.Inaddition,asinglediskherniationmayinvolvetwonerveroots.ThisappliesparticularlytotheL4-L5disk,whichmay compress not only the L5 root but also the S1 root, particularly if theherniation is in themidline.Disk herniation occasionally occurs atmore thanonelevel,givinganatypicalneurologicpattern.

FIGURE2-35L4/L5diskherniationcompressingtheL5nerve.

TABLE2-1UNDERSTANDINGHERNIATEDLUMBARDISKSROOTDISKMUSCLES REFLEX SENSATION EMG MYELOGRAML4 L3-

L4Tibialisanterior

Patellar Medialleg Fibrillationorsharpwavesintibialisanterior

BulgeinspinalcordadjacenttoL3-L4

L5 L4-L5

Extensorhallucislongus

None(tibialisposterior)

Lateralleganddorsumoffoot

Fibrillationorsharpwavesinextensorhallucislongus†

BulgeinspinalcordadjacenttodiskL4-L5

S1 L5-S1*

Peroneuslongusandbrevis

Achillestendon

Lateralfoot Fibrillationorsharpwavesinperoneuslongusandbrevis‡

BulgeinspinalcordadjacenttodiskL5-S1

*Mostcommonlevelofherniation.

†Extensordigitorumlongusandbrevis,medialhamstring,gluteusmediusmuscles.‡Flexorhallucislongus,gastrocnemius,lateralhamstring,gluteusmaximusmuscles.EMG,electromyogram.

FIGURE2-36AherniateddiskbetweenvertebraeL3andL4involvestheL4nerveroot.

LowBackDerangementversusHerniatedDiskPatientsfrequentlydevelop“lowback”painafterliftingheavyobjectsorfalling,or after a violent automobile accident that throws or twists them around theinterior of the car. These patients complain of back pain (point tenderness orpainacrossthelowerlumbarspine)withradiationtovaryingdegreesaroundtheposteriorsuperioriliacspinesanddownthebackoftheleg.

Complaints of a generalized backache or low back derangement withoutneurologic involvement can be differentiated from those with neurologicinvolvement by testing the neurologic levels innervating the lower extremity.

The tests should be repeated with each visit, because a loss of function notapparentintheinitialexamination;afurtherlossofmusclestrength,reflex,orsensation in the involvedneurologic level;or an improvement from the initialfindings(asaresult,perhaps,oftreatment)mayoccur.

Unlessthereisevidenceeitherofanalterationinreflex,sensation,ormotorpower or of positive findings on electromyogram, nonsurgical conservativetherapy including physical therapy, injections, and medication managementshouldcontinuedespitepatientpressureforachangeintreatment.

Although neurologic involvement of a herniated disk is most oftenmanifestedby thealterationofonlyoneor twosigns, there shouldbeenoughinformation to help pinpoint the involved neurologic level. Certainly, theelectromyogramandmagneticresonanceimaging(MRI)canbeusedasfurtherdiagnostictools.Butyourclinicaljudgment,basedonthephysicalexaminationof the patient, will most often allow you to make the proper neurologicdiagnosisandprescribethecorrecttreatment.

FIGURE2-37AherniateddiskbetweenvertebraeL4andL5involvestheL5nerveroot.Thisisthesecondmostcommonlevelofdiskherniationinthelumbarspine.

SpondylolysisandSpondylolysthesisSpondylolysis refers to the lytic line that crosses the pars interarticularis, thearea between the superior and the inferior articulating processes, or, moreprecisely, the point at which the inferior articulating process approaches thepedicle(Fig.2-40).Asaresultofthispathology,theinvolvedvertebramayslipforward on the vertebra immediately inferior to it. This forward slippage iscalled spondylolysthesis. Although the etiology of the defect of the parsinterarticularis is still unknown, it is commonly believed to be the result of afracture due to repeated stress. Because of the frequency of L5-S1spondylolysthesis with involvement of L5-S1 nerve roots, the hamstrings,supplied medially by L5 and laterally by S1, may well go into spasm. Bothsensation and reflex usually remain normal, unless there is an associatedherniated disk.Occasionally, spondylolysthesismayoccur evenwith an intactparsinterarticularisinpatientswithdegenerativearthritis.However,thisisveryunusual.

Thedegreeofforwardslippageismeasuredclinicallybytherelationshipofthe superior vertebra to the inferior vertebra (the superior vertebra slipsforward).Aslipofupto25percentistermedafirst-degreeslip,25to50percenta second-degree slip, and 50 to 75 percent a third-degree slip. Any greaterslippageis termedafourth-degreeslip.Thevertebramostcommonly involvedin spondylolysis and spondylolysthesis is the L5 vertebra. The second mostcommonisL4.

FIGURE2-38AherniateddiskbetweenvertebraeL5andS1involvestheS1nerveroot.Thisisthemostcommonlevelofdiskherniationinthelumbarspine.

FIGURE2-39MRI:aherniateddiskatL5,S1.

FIGURE2-40Parsinterarticularis.

Thedegreeofpainthatthepatientexperiencesisnotnecessarilyrelatedto

thedegreeofslippage,soapatientwithafirst-degreeslipmayfeelgreaterpainthanapatientwithafourth-degreeslip,whomay,infact,feelnopainatall.

An increase of symptoms in patients with spondylolysis orspondylolysthesiscanoftenbetheresultofanassociatedherniatedlumbardisk.The incidenceof aherniateddisk isgreater inpatientswith spondylolysthesisthanthatinthegeneralpopulation.Thediskherniationusuallyoccursonelevelabovethebonypathology.Forexample,ifthereisabonydefectatL5,thediskbetweenL4andL5istheonemostlikelytoherniate.TheinvolvementoftheL5nerverootmayproduceassociatedneurologicfindings,suchaspositivestraightlegraising,toeextensorweakness,anddiminutionofsensationonthedorsumofthe foot. Although such involvement usually stems from an associatedherniation, the nerve root may also become impinged directly from aspondylolysthesis.

Spondylolysis and spondylolysthesis are frequent causes of teenagebackache; the patient usually complains of back pain, particularly after sportsactivities.

Note that spondylolysis has a characteristic look on an x-ray (Figs. 2-41and2-42).

FIGURE2-41Schematicdrawingofanobliqueroentgenogramofthelumbarspine,showingthecharacteristic“scottydog”lookofitsposteriorelements.Notethatthedefectintheparsinterarticularisappearstobeacollararoundthedog’sneck.

FIGURE2-42Spondylolysis.

HerpesZosterHerpes zoster (shingles) is a viral disease that usually involves a single,unilateral dermatome. Thoracic roots are most commonly involved. Painfrequentlyprecedestheappearanceoftheskinlesionandfollowsthedistributionofthenerveroot,withoutcrossingthemidline.Thelevelinvolvedcanbelocatedthroughappropriatesensorytestingandevaluationoftheleveloftheskinlesion.

PoliomyelitisPoliomyelitis is an acuteviral infectiousdisease thatmay inflict temporaryorpermanentdestructivechangesinmotorfunction.Itinvolvesthedestructionoftheanteriorhorncellsofthespinalcord.Poliomyelitisusuallyattacksyoungerpatients,causingmotorparalysisandatrophy. Itdoesnotaffect sensation,andreflexes, although diminished, are usually present, because the reflex arcsremainintactunlessalltheanteriorhorncellsaredestroyed(Fig.2-43).

Althoughitslesionliesinthecord,theclinicalappearanceofpoliomyelitismaybesimilartothatofanerverootlesion,becausethevirusdestroysthecellsof the nerve root. At least 50 percent of the anterior horn cells in the levelsinnervating a particular muscle must be involved before there is any clinicalevidence ofmuscleweakness (according toW. J.W. Sharrard). Poliomyelitisattackstheanteriorhorncellssegmentally—itdoesnotsimplyinvolvealllevelsinanarea—anditmayskiplevels,leavingthemfreeofpathology.Thisleadstoa smaller degree of involvement for muscles that are innervated by severallayers.Forexample,thequadricepsmuscle,whichisinnervatedbyL2-L4,doesnotexperienceanysignificantweaknessunless50percentof theanteriorhorncells of all three levels are involved. Conversely, the tibialis anteriormuscle,whichisinnervatedmainlybyL4,isaffectedbytheinvolvementof50percentoftheanteriorhorncellsofthatlevel,causingtherelativelycommonproblemoffoot drop. If the anterior horn cells of the 5th lumbar level are involved,weakness of the gluteus medius muscle, the medial hamstrings, and the toeextensors may occur. If the anterior horn cells of the 1st sacral level areinvolved, theremay beweakening of the gluteusmaximusmuscle, the lateralhamstring,andtheperoneiandcalfmuscles.

FIGURE2-43Anteriorhorncelllossleadingtoclinicalmuscleweakness.

Through vaccination, poliomyelitis has been practically eliminated as aseriousproblem.

MUSCLE NEUROLOGICLEVEL* NERVEHipflexors L1,L2,L3Hipadductors L2,L3,L4 ObturatornerveQuadriceps L2,L3,L4 FemoralnerveTibialisanterior L4,L5 DeepperonealnerveTibialisposterior L4,L5 PosteriortibialnerveGluteusmedius L4,L5,S1 SuperiorglutealnerveMedialhamstrings L4,L5,S1 Sciaticnerve,tibialportionExtensordigitorumlongus L5,S1 DeepperonealnerveExtensorhallucislongus L5,S1 DeepperonealnervePeronei L5,S1,S2 SuperficialperonealnerveCalf L5,S1,S2 TibialnerveLateralhamstring L5,S1,S2 Sciaticnerve,tibialportionGlutealmaximus L5,S1,S2 InferiorglutealnerveFlexorhallucislongus S1,S2 TibialnerveFlexordigitorumlongus S1,S2 TibialnerveToeintrinsics S2,S3 LateralandmedialplantarnervesPerineum S2-S4

*AccordingtoSharrard.Predominantneurologiclevel.

SpinalCordLesionsbyNeurologicLevel

Theacuteinjuriesleadingtotetraplegiaandparaplegiapresentgreatproblemsinbothearlydiagnosisofthelevelsofneuralinvolvementandprognosticationoffuture function. In today’s society, where potentially debilitating occurrences,includingwar, auto and industrial accidents, and contact sports, are common,thereisaneedforaconcisesystemofearlyneurologicexamination.Traumaticpathologyofanykindthataffectsthespineandspinalcordmustbediagnosedimmediately and must be accurately and promptly treated. The key tomanagementofspinalinjuriesisimmediateprotectionofthespinalcord,evenifan immediate examination is not performed. Without immediate protection,incomplete lesions of the cord can progress to complete lesions, and partiallycontusednerverootsmaybetotallylost.

Spinal injuriesmayoccuratany level.Each levelatwhichan injurycanoccurgivesspecialproblems:acute injuries to thecervicalspinemayresult indeath or tetraplegia; injuries to the thoracic spine usually lead to spasticparaplegia;andinjuriestothelumbarspine(caudaequinainjuries)canresultinvaryingdegreesof flaccid lowerextremityparalysis.Thefollowingdiscussiondealswiththesethreezonesandwithmethodsofexaminationthathelpestablishapreciselevelofneuralinvolvement.

CervicalCordLesions:Tetraplegia

Tetraplegia, or quadriplegia as it is more commonly known, means paralysisinvolvingallfourextremities.Thelesionthatcausessuchparalysisoccursinthecervicalspine.

In an analysis of tetraplegia, establishment of the level of neuralinvolvementandevaluationofitsdegree(whetherthecordlesioniscompleteorincomplete) areofprimaryconcern.Both these factorsmustbeknownbeforethere can be any attempt at prediction of recovery of neurologic function orbeforeanyeffectiveprogramoftherapeutictreatmentandrehabilitationcanbeplanned.Themorerapidtherateofreturnofspinalcordfunction,thegreatertheamountofrecoveryand,conversely,theslowertherateofreturn,thesmallertheamount of recovery.This rule of thumbmakes it easier to estimate the futurepossibilityofbothambulationandbladderandbowelfunction.Because,atthebeginning,thepatientmaybeinastateofspinalshock(diaschisis),fromwhichsomeneural recoverymayoccur,a thoroughneurologicexamination, repeatedevery2 to4hours for the first 48hours,maybegin toprovide someanswersaboutthepotentialforrecovery.Eachexaminationmustincludemuscletesting,sensory testing, and reflex testing to permit a complete evaluation of thepossibilityofcordreturn.

EvaluationofIndividualCordLevels:C3-T1If the cervical cord is completely transected, complete paralysis of the lower

extremitiesoccurs,butthedegreeofparalysisoftheupperextremitiesdependson the neurologic level involved.Although some cervical cord lesions are, inreality,incompleteorpartial(sothatsomefunctionremainsbelowthelevelofthelesion),weshalldiscussthesignsasifeachcordlesioniscomplete,becausetherealissueistodeterminethelevelofinjury.

Spinal shock and associated muscle flaccidity usually pass between 24hoursandthreemonthsaftertrauma.Spasticityandclonussetinandgraduallyincrease in intensity. The deep tendon reflexes become exaggerated andpathologicreflexesappear.

NeurologicLevelC3(C3Intact)AneurologiclevelofC3meansthatthethirdcervicalrootisintact,whereasthefourthisnot.NeurologiclevelC3correspondstovertebrallevelC3,C4(Fig.3-1).

MotorFunctionThere is nomotor function in the upper extremities; the patient is completelytetraplegic.Musclesareflaccidasaresultofdenervationandspinalshock.Afterspinal shock has worn off, the muscles will demonstrate varying degrees ofspasticresponse.BecausethediaphragmissuppliedlargelybyC4,thepatientisunable to breathe independently, and will die without artificial respiratoryassistance. Sometimes, in what at first appears to be a C3 level, C4 laterrecovers,withareturnofdiaphragmaticfunction.

FIGURE3-1Tetraplegia:neurologiclevelC3.

SensationThereisnosensationintheupperextremitiesorbelowalinethreeinchesabovethenippleontheanteriorchestwall.

ReflexesInthepresenceofspinalshock,alldeeptendonreflexesareabsent.Whenspinalshock has worn off, they will become brisk to exaggerated and pathologicreflexesmaybeevident.

NeurologicLevelC4(C4Intact)

The4th cervical cord segment remains intact.The lesion liesbetween the4thand5thcervicalvertebrae(Fig.3-2).

MotorFunctionThemusclesoftheupperextremityarenonfunctional.BecauseC4isintact,thepatient can breathe independently and shrug the shoulder. But the lack offunctioning intercostal and abdominal muscles keeps the patient’s respiratoryreservelow,althoughprobablyadequateforthereducedleveloffunction.

Sensationispresentontheupperanteriorchestwall,butnotintheupperextremities.

ReflexesInitially,alldeeptendonreflexesareabsent,butthepassingofspinalshockmay

bringchanges.

NeurologicLevelC5(C5Intact)A lesion at this level leaves C5 intact. Because this is the first cord level tocontributetotheformationofthebrachialplexus,theupperextremitywillhavesomefunction(Fig.3-3).

MotorFunctionThe deltoid muscle and a portion of the biceps muscle are functioning. Thepatientisabletoperformshoulderabduction,flexion,andextension,aswellassome elbow flexion. However, all these motions are weakened because themuscles governing these movements usually have contributions from the C6nerve root. The patients cannot propel a wheelchair by themselves and theirrespiratoryreserveislow.

Sensationisnormalovertheupperportionoftheanteriorchestandinthelateralaspectofthearmfromtheshouldertotheelbowcrease.

ReflexesBecausethebicepsreflexisprimarilymediatedthroughC5,itmaybenormalorslightly decreased. As spinal shockwears off and elements of C6 return, thereflexmaybecomebrisk.

NeurologicLevelC6(C6Intact)InvolvementisatskeletallevelC6-C7(Fig.3-4).

MotorFunctionBecause both C5 and C6 are intact, the biceps and the rotator cuff musclesfunction.Themostdistal functionalmusclegroup is thewrist extensorgroup;theextensorcarpiradialislongusandbrevis(C6)arebothinnervated(althoughthe extensor carpi ulnaris—C7—is still involved). The patient has almost fullfunction of the shoulder, full flexion of the elbow, full supination and partialpronationoftheforearm,andpartialextensionofthewrist.Thestrengthofwristextensionisnormal,becausepowerforextensionispredominantlysuppliedbytheextensorcarpiradialislongusandbrevis.

Respiratory reserve is still low. The patient is confined to a wheelchair,whichcanbepropelledoversmooth,levelsurfaces.

SensationThe lateral sideof theentireupperextremity,aswellas the thumb, the index,andhalfofthemiddlefinger,hasanormalsensorysupply.

ReflexesBoththebicepsandthebrachioradialisreflexesarenormal.

NeurologicLevelC7(C7Intact)InvolvementisatvertebrallevelC7-T1(Fig.3-5).

MotorFunctionWiththeC7nerverootintact,thetriceps,thewristflexors,andthelongfingerextensors are functional. The patient can hold objects, but grasp is extremelyweak.Although he is still confined to awheelchair, the patientmay begin toattemptparallelbarandbraceambulationforgeneralexercise.

SensationC7haslittlepuresensoryrepresentationintheupperextremity.NoprecisezoneforC7sensationhasbeenmapped.

ReflexesThebiceps(C5),brachioradialis(C6),andtriceps(C7)reflexesarenormal.

NeurologicLevelC8(C8Intact)InvolvementisatskeletallevelT1-T2(Fig.3-6).

MotorFunctionTheupper extremity isnormal, except for the intrinsicsof thehand.Thus, allupper extremity motions except finger abduction, finger adduction, and thepinchmechanismof the thumb, index, andmiddle fingers are intact.Grasp isdifficult,becausethehandisintrinsicminusorclawed.

SensationThelateralaspectoftheupperextremityandtheentirehandhasnormalsensoryawareness. Sensation on the medial side of the forearm is normal to severalinchesbelowtheelbow.

ReflexesAllupperextremityreflexesareintact.

NeurologicLevelT1(T1Intact)InvolvementoccursatskeletallevelT2-T3.

MotorFunctionInvolvementatneurologiclevelT1resultsinparaplegia.Theupperextremityisfully functional. The brachial plexus’ neurologic supply (C5-T1) is intact,whereas the lowerextremities arepartiallyorwhollyparalyzed,dependingonthedegreeofcorddamageatthatlevel.Thepatientcanambulateinavarietyofwayswithcorrectbracing,butawheelchairisstillthemostpracticalmeansofmoving about.A T1 paraplegic can drag-towith crutches and bracing but hecannot assume the erect positionwithout somehelp.Trunk stability is absent,andtheenergycostofambulationismarkedlyincreased.Therefore,ambulationisnotfunctional,butisusefulasexercise.

SensationTheanteriorchestwallaslowasthenippleandtheentireupperextremityhavenormalsensation.

ReflexesThereflexesintheupperextremityarenormal.

UpperMotorNeuronReflexesPathologicreflexesappearintheupperandlowerextremitiesinassociationwithtetraplegia. Hoffmann’s sign can be elicited in the upper extremity and, ifpresent,isanindicationofanuppermotorneuronlesionandcanbeelicitedin

theupperextremity.To test forHoffmann’s sign, nip the nail of themiddle finger.Normally

there should be no reaction at all.A positive reaction produces flexion of theterminalphalanxof the thumbandof thesecondand thirdphalanxofanotherfinger(Fig.3-7).

FIGURE3-7Hoffmann’ssign,indicatinganuppermotorneuronlesion.

ClinicalApplicationFracturesandDislocationsoftheCervicalSpineInjuriestothecervicalspineareamajorcauseoftetraplegia.Thetypesofinjuryinclude flexion injuries (compression fractures), hyperextension injuries, andflexion-rotationinjuries(cervicalfacetdislocations).

On occasion, the neurologic level involved does not correspond to theskeletal level. Thus, in a fracture-dislocation of the 5th and 6th cervicalvertebrae,theC6neurologiclevelmayremainfunctional.Eachpatientmustbeevaluatedonanindividualbasis.

FractureofC1The C1 or Jefferson fracture is a bursting fracture of the ring of C1, whichusuallydecompressesthecord.Thefracturecommonlyresultsfromafall,withthe patient landing on the head. If the patient survives, there are usually nopermanentneurologicfindings(Figs.3-8and3-9).

FIGURE3-8Jeffersonfracture,aburstingfractureoftheringofC1.

FIGURE3-9Jeffersonfracture.

FractureofC2

TheC2orhangman’sfractureisaburstingfracturethatseparatesthebodyofC2from its posterior elements, thereby decompressing the cord. If the patientsurvives,thereareusuallyonlytransientneurologicfindings(Figs.3-10and3-11).

OdontoidFractureA fracture at the base of the odontoid commonly results from trauma. Thepatientusuallysurvives.Theremaybetransientneurologicfindings,butwithouttheestablishmentoftheinvolvementofaspecificneurologiclevel.Onoccasion,if the trauma is severe enough, the patient dies. However, there is usuallyenough space in the cervical canal to allow for partial displacement of theodontoid(Figs.3-12and3-13).

FIGURE3-10Hangman’sfracture,afracturethatseparatesthebodyofC2fromitsposteriorelements.

FracturesofC3-C7Compression fractures arecausedbyhyperflexion injuriesof theneckwhena

verticalforcerupturestheendplatesofthevertebraandshattersthebody.Thisburstingfractureoccursinboththecervicalandlumbarspinesandmayinvolveboththenerverootandthecorditself(Fig.3-14).AcompressionfractureoftheC5vertebra, themostcommonfractureof thecervicalspine, involvesmostofthebrachialplexusandmayresultintetraplegia.Compressionfracturesareeasytodiagnoseonx-ray(Fig.3-15).

FIGURE3-11Hangman’sfracture.

Hyperextension injuries of theneck are causedbyhyperextension forces,such as the acceleration injury caused by a rear-end automobile collision. Ahyperextension injury is essentially a soft tissue injury, unlike a compressioninjury, which fractures the body of the vertebra; the anterior longitudinal

ligamentisusuallyrupturedandthecordmaywellbecomeinvolved.Becauseitis a soft tissue injury, the hyperextension injurymaynot be obvious on x-ray(Fig.3-16).

Cervicalfacetjointdislocationsareflexion-rotationinjuriesthatmaycauseneurologicproblems.Aunilateralfacetdislocationproducessomenarrowingofthe spinal canal and neural foramen. Because a unilateral facet dislocationusuallyresultsinlessthan50percentanteriordislocationofthevertebralbody,approximately75percentofcaseshavenoneurologicinvolvement,becausethenarrowingisnotsufficienttoaffectthecord(Figs.3-17to3-20).

Bilateral facet dislocations produce far greater narrowing of the spinalcanal thanunilateral dislocationsbecause,withboth facetsdislocated, there isusually greater than 50 percent anterior dislocation of the vertebral body.Because of this greater degree of dislocation, approximately 85 percent ofpatientssufferneurologiclesions.Becausethecervicalspinedependsprimarilyon ligaments for its stability, bilateral facet dislocations, which cause theligamentstotear,rarelyhealwithsufficientstrengthtoreinstatespinalstability;unless appropriate treatment is undertaken, there is a risk of further damagesecondarytoanynumberofpossibleaccidents.Bilateraldislocationsmayoccuratany level,but theyaremostcommonatC5-C6, the levelaroundwhich themostmovement takes place (except for the specialized articulation at C1-C2)(Figs.3-21and3-22).

FIGURE3-12Odontoidfracture.

FIGURE3-13Odontoidfracture.

FIGURE3-14Cervicalcompressionfracture,causedbyhyperflexionoftheneck.

FIGURE3-15Cervicalspinecompressionfracture.

ActivitiesofDailyLiving

RespirationFrom this description of cord lesions, it should be apparent that a completetransectionofthecordatneurologiclevelC3orhigherisincompatiblewithlife,

unlessthepatientispermanentlyventilated.InvolvementatneurologiclevelsC4toC5maycausedegreesofrespiratoryinsufficiencythatmaythreatenlifeinthepresenceofrelativelymildpulmonarydisease.

FIGURE3-16Hyperextensioninjuryofthecervicalspine.

FIGURE3-17Painassociatedwithfacetjointdislocation.

FIGURE3-18Unilateralfacetjointdislocation.(Hoppenfeld,S.:PhysicalExaminationoftheSpineandExtremities.Norwalk,CT:Appleton-Century-Crofts,1976.)

WheelchairC6isthehighestneurologiclevelthatleavessufficientinnervationoftheupperextremity to permit independent manipulation of a wheelchair. However,independent transfer intoandoutof thewheelchair is stilldifficultbecauseofthelackoffunctionofthetricepsmuscle.Anactivetricepsisneededtohelpliftthebodyfortransfer.

CrutchesCompletecordlesionsatneurologiclevelC8andaboveareincompatiblewith

theuseofcrutchesbecausetheintrinsicmusclesofthehand,neededforstronggrip on the crutches, are nonfunctioning. Functional walkingwith crutches ismademoredifficultbothbecauseoftheneedtoexpendtwotofourtimesmoreenergy than in normal ambulation and because of a decreased respiratoryreserve.Attemptstoencouragewalkingwithbracesandothersupportsarealsorarelysuccessful.

FIGURE3-19A,BInaunilateralfacetjointdislocation,thereislessthan50percentanteriordislocationofthevertebralbody.

Note that this is true of complete cord lesions; partial cord lesions showvaryingpatternsofneurologicdeficiency.Eachpatientmustbeassessedasanindividual(Fig.3-23).

FIGURE3-20Unilateralfacetjointdislocation.GradeIanteriordislocationofthevertebralbody.

HerniatedCervicalDisksAlthoughherniatedcervicaldisksoftencauseneurologicrootinvolvement,thecervical canal is sufficiently large to accommodate the herniated diskwithoutsignificantcorddamage,andtetraplegiararelyoccurs.However,minordegreesofcorddamage—uppermotorneuronlesions—mayresultfromalargemidlineherniation. They are usually first recognized as a diminution in sensation ofpositionandvibration in the lower extremities. Inmoreadvancedcases, theremaybeactualmuscleweaknessandanincreaseinthedeeptendonreflexes,aswellasearlybladdersymptoms.

FIGURE3-21A,BBilateralfacetjointdislocation,resultingingreaterthan50percentanteriordislocationofthevertebralbody.

FIGURE3-22Bilateralfacetjointdislocation.GradeIIIanteriordislocationofthevertebralbody.

TumorsoftheCervicalSpineTumorsof thecervicalcordarespace-occupyinglesions.Theymaypresentaslocal pain in the spine, and may also radiate pain to the extremities. Theanatomic location of the tumor can usually be ascertained by a neurologicevaluationoftheextremity.Forexample,atumorofthecervicalcordinvolvingtheC6-C7 neurologic segmentmay cause anesthesia of themiddle finger, anabsenceofthetricepsreflex,andweaknessoffingerextensionandwristflexion.Primarytumorsofthecordrarelygivepreciseneurologiclevelsofinvolvement.

Metastatictumorsinthevertebraeofthecervicalspinearenotuncommon.

Primarybreastandlungtumorsfrequentlymetastasizetothespine.Asboneisdestroyed, vertebral collapse and angulation take place and tetraplegia occurs.Theneurologiclevelofinvolvementusuallycorrelateswiththex-rayfindings.

TuberculosisoftheSpineTuberculosis of the spine causes gibbus formation through the destruction ofbone. The spinal angulation may ultimately cause cord compression andtetraplegia, but the process is far slower than that of trauma. Frequently,neurologicrecoveryoccursaftersurgicaldecompressionandchemotherapy.

TransverseMyelitisTransversemyelitis refers to an inflammatory process in which a spinal cordlesionextendinghorizontallyacrossthecordislimitedlongitudinallytooneor,at most, a few spinal segments. Ascending myelitis occurs when the lesionspreadsproximally.

FIGURE3-23Thefindingsresultingfromacompletelesiondependontheanatomicconfigurationofthedestructionofneuraltissueataparticularlevel.

Transverse myelitis may occur spontaneously and rapidly following avaccination, an infectious illness, or trauma.Although sensory andmotor lossoccurs below the lesion, complete anesthesia is rare. Flaccid paralysis occursinitially,butquicklyrevertstospasticparalysis.

The neurologic level of involvement can usually be delineated byneurologic level testing of sensation, motor power, and reflexes. The highestlevelofsensorylossusuallycorrespondstothesegmentalsiteofthecordlesion.

SpinalCordLesionsBelowT1,IncludingtheCaudaEquina

ParaplegiaParaplegiaisthecompleteorpartialparalysisofthelowerextremitiesandlowerportionofthebody.Itismostfrequentlycausedbytraumaticinjurytothespine,but may also derive from various diseases such as transversemyelitis, cysticlesionsofthecord,andPott’sparaplegia(causedbytuberculosis),aswellasahost of other pathologies. It occurs rarely from surgical correction of suchthoracicproblems as scoliosis, as a result of the loss of the appropriate bloodsupplytothespinalcord,andfromtheexcisionofaherniatedthoracicdisk.

Thecaudaequinacomprises the rootsof all spinalnervesbelow the firstlumbar vertebra.Cauda equina is a descriptiveLatin term because the nervesresembleahorse’stail,andrarelyresultinfullparalysisofthelowerextremities

The following descriptions assume that a complete lesion exists. Often,however, lesions are incomplete; the neurologic findings for each individualpatientmustbecarefullydetermined,forinvolvementmayvaryconsiderably.

NeurologicLevelsT1-T12Thelevelofneurologicinvolvementcanbedeterminedbytestsofmotorpowerandsensation.Thelatteriseasierandmoreaccurate.

MuscleFunctionThe intercostalmuscles, aswell as the abdominal andparaspinalmuscles, aresegmentallyinnervated.Intercostalmotionduringbreathingimpliesneurologicintegrity;alackofmotionimpliesinvolvement.Theabdominalandparaspinal

musclescanbesimilarlyevaluated,fortheyarebothsegmentallyinnervatedbyT7-T12(L1).Totestfortheintegrityoftheirinnervation,havethepatientdoahalf sit-up as you palpate the anterior abdominalwall.As the patient sits up,notewhether the umbilicus is pulled toward any of the four quadrants of theabdomen. If the umbilicus is pulled in one direction, the opposing flaccidmusclesaredenervated(Beevor’ssign)(Fig.2-1).NotethattheumbilicusisthedividinglinebetweenT10aboveandT11below.Obviously,thistestshouldnotbe performedduring the acute stages of thoracic lesions orwith patientswhohaveunstablespines.

SensationSensoryinnervationmaybedeterminedinaccordancewiththechart(Fig.4-1).Specialskinlandmarksthatmarksensoryareasareasfollows:1. Nippleline—T42. Xiphoidprocess—T73. Umbilicus—T104. Groin—T12

L1NeurologicLevel(L1Intact)

MuscleFunctionThereiscompleteparalysisofthelowerextremities,withtheexceptionofsomehipflexionfrompartialinnervationoftheiliopsoas(T12,L1-L3)(Fig.4-2).

SensationThere is no sensation below the L1 sensory band, which extends over theproximalthirdoftheanterioraspectofthethigh.

ReflexesThe patellar and Achilles tendon reflexes are absent when spinal shock ispresent.Asspinalshockwearsoff,thereflexesbecomeexaggerated.

BladderandBowelFunctionThebladder(S2-S4)doesnotfunction.Thepatientcannoturinate inastream.Theanusis initiallypatulous,andthesuperficialanalreflex(S2-S4)isabsent.

As spinal shock wears off, the anal sphincter contracts and the anal reflexbecomeshyperactive.

FIGURE4-1Sensorydermatomesofthetrunk.

MuscleFunctionThere isgoodpower inhip flexionbecause the iliopsoas isalmostcompletelyinnervated. The adductor muscles are partially innervated (L2-L4) and showdiminished power. Although the quadriceps (L2-L4) are partially innervated,there is no clinically significant function. No other muscles in the lowerextremity have innervation, and the unopposed action of the iliopsoas and

adductorstendstoproduceaflexionandslightadductiondeformity.

SensationThereisnosensationbelowtheL2sensoryband,whichendstwo-thirdsofthewaydownthethigh.

ReflexesThepatellarreflexreceivesinnervationfromL2toL4,buttheL2contributionissmall.

BladderandBowelFunctionThereisnovoluntarycontrol.

MuscleFunctionIn addition to the iliopsoas and adductors, the quadriceps (L2-L4), althoughslightlyweak,showsignificantpower.Noothermusclegroupsarefunctioning.Thus,thehiptendstobecomeflexed,adducted,andexternallyrotatedwhilethekneeremainsextended.

SensationSensationisnormaltotheleveloftheknee(L3dermatomeband).

ReflexesThepatellarreflex(L2-L4)ispresent,butdecreased.TheAchillestendonreflexisabsent.

BladderandBowelFunctionThereisnovoluntarycontrol.

MuscleFunction

Muscle function at the hip and knee is the same as in L3 neurologic lesionsexcept that quadriceps function is now normal. The only functioning musclebelow theknee is the tibialis anterior (L4),whichcauses the foot todorsiflexandinvert.

FIGURE4-2InnervationoftheiliopsoasT12-L3.

SensationInadditiontotheentirethigh,themedialsideofthetibiaandfoothassensation.

ReflexesThepatellarreflex(predominantlyL4)isnormal;theAchillestendonreflex(S1)isstillabsent.

BladderandBowelFunctionThereisnovoluntarycontrolofeitherfunction.

MuscleFunctionThe hip still has a flexion deformity, because the gluteus maximus does notfunction. Innervation of the gluteusmaximus is derived fromL5, S1 and S2.Thegluteusmedius(L1-S1)haspartialfunction;itcounteractstheactionoftheadductors.Thequadricepsarenormal.

Thekneeflexorsfunctionpartiallywiththemedialhamstrings(L5)presentandthelateralhamstrings(S1)absent.

The foot dorsiflexors and invertors function. Because the plantar flexorsandevertorsarestillabsent,thefoottendstodevelopacalcaneus(dorsiflexion)deformity.

SensationSensationisnormalinthelowerextremity,withtheexceptionofthelateralsideandplantarsurfaceofthefoot.

ReflexesThepatellarreflexisnormal.TheAchillestendonreflexisstillabsent.

BladderandBowelFunctionThereisnovoluntarycontrolofeitherfunction.

S1NeurologicLevel(S1Intact)

MuscleFunctionThe hip muscles are normal, with the exception of slight gluteus maximusweakness.Thekneemusclesarenormal.Thesoleusandgastrocnemius(S1,S2)areweak, and the toes show clawing as a result of intrinsicmuscleweakness(S2,S3).

SensationSensationinthelowerextremityisnormal.Thereisperianalanesthesia.

ReflexesThe patellar and Achilles tendon reflexes are normal, because the S2contributiontotheAchillestendonreflexissmall.

BladderandBowelFunctionThereisstillnovoluntarycontrolofeitherfunction.

UpperMotorNeuronReflexesPathologicReflexesPathologic reflexescanbeelicited in the lowerextremities inassociationwithparaplegia.Babinski’s sign andOppenheim’s sign are two pathologic reflexesthatindicateanuppermotorneuronlesion.

Babinski’sSignElicit the plantar response by running a sharp instrument across the plantarsurfaceof the foot, andalong thecalcaneusand lateralborderof the forefoot.Normally, in a negative reaction, the toes plantarflex. A positive reaction(Babinski’ssign)occurswhenthegreattoeextendsastheothertoessplay(Fig.4-3). This sign indicates an upper motor neuron lesion—a corticospinal tractinvolvement.Toascertain the levelof the lesion,correlate thissignwithotherneurologicfindings.Inyounginfants,thepresenceofBabinski’ssignisnormalrather than pathologic. However, this response should disappear by 12 to 18monthsofage.

Oppenheim’sSignToelicitOppenheim’ssign,runyourfingeralongthecrestofthetibia.Normallythereshouldbenoreactionatall,orthepatientshouldcomplainofpain.Underabnormalcircumstances,thereactionisthesameasitisinplantarstimulation:the great toe extends as the other toes splay (Oppenheim’s sign) (Fig. 4-4).Oppenheim’ssignisnotasreliableasBabinski’ssignandshouldbeusedasaconfirmationofapositiveBabinski’ssign.

FIGURE4-3Babinski’ssign.

NormalSuperficialReflex

CremastericThelackofthecremastericreflexmaybedueeithertothelossofthereflexarcor to an upper motor neuron lesion. However, absence of the reflex inassociationwiththepresenceofapathologicreflex(Babinski’sorOppenheim’ssigns)supportsthediagnosisofanuppermotorneuronlesion.

FIGURE4-4Oppenheim’ssign.

FIGURE4-5Thecremastericreflex.(Hoppenfeld,S.:PhysicalExaminationoftheSpineandExtremities.Norwalk,CT:Appleton-Century-Crofts,1976.)

Toelicitthesuperficialcremastericreflex,stroketheinnersideoftheupperthigh with the sharp end of a neurologic hammer. If the reflex is intact, thescrotal sac on that sidewill be pulled upward as the cremastermuscle (T12)contracts. If the cremasteric reflex is unilaterally absent, there is probably alowermotorneuronlesionbetweenL1andL2(Fig.4-5).

ClinicalApplicationFurtherEvaluationofSpinalCordInjuries

CompleteorIncompleteLesion

Thepossibilityofcord return,andwhateverpartial functional recovery itmayprovide,dependsonwhetherthelesioniscompleteorincomplete,whetherthecord is completely severed or only partially severed or contused. Injuries inwhich no function returns over a 24-hour period are assumed to be completelesions, where no return of cord function will occur. A complete neurologicexaminationisneededtoconfirmsuchadiagnosis.If,however,thereispartialreturn of function in the initial period, the lesion is probably incomplete, andmore functionmay eventually return. Functionmust return at more than oneneurologic level to support such a diagnosis, however, because return at onlyonelevelmaysimplyindicate that thenerverootat the levelof the lesionhasbeenpartiallydamagedorcontused.Suchsingle-levelreturngivesnoindicationastowhetherthelesionbelowitiscompleteorincomplete.Therecoveryofthissinglenerverootisconsideredtobearootlesion(ratherthanacordlesion)oftherootoriginatingjustproximaltotheinjuredportionofthecord.Functionalreturn of muscle strength from such an injury may occur at any time;prognostication for root return is good as late as six months after the initialinjury.

SacralSparingThebestindicatorofthepossibilityofcordreturnissacralsparing,inwhichthesacralnervesarepartiallyorwhollyspared injurybecauseof their locationonthe periphery of the cord. Evidence of sacral sparing is evidence of anincomplete lesion. It enhances the possibility of partial or complete return ofmotorpoweraswellasofbladderandbowelfunction.

Sacralsparingcanbeevaluatedthroughthreetestsofmotor,sensory,andreflexinnervation:1. Muscletestingofflexionofthegreattoe(S1innervation)2. Sensorytestingoftheperianalarea(S2-S4)3. Reflextestingoftheanalsphinctermuscle(S2-S4)

Becausethebladderandbowelareinnervatedbythesacralnerves(S2-S4),testing of these three areas gives a valid indication of the degree of sacralsparingandthepossibilityofreturnoffunction(Fig.4-6).

FlaccidityandSpasticityImmediatelyafteranytraumacausingtetraplegiaorparaplegia,thespinalcordexperiences spinal shock, resulting in the loss of reflexes innervated by theportionofthecordbelowthesiteofthelesion.Thedirectresultofspinalshock

isthatallthemusclesinnervatedbythetraumatizedportionofthecordandtheportionbelow the lesion, aswell as thebladder,become flaccid.Spinalshockwears off between 24 hours and threemonths after injury, and spasticitymayreplaceflaccidityinsomeorallofthesemuscles.Spasticityoccursbecausethereflexarctothemuscleremainsanatomicallyintactdespitethelossofcerebralinnervationandcontrolviathelongtracts.Duringspinalshock,thearcdoesnotfunction; as the spine recovers from shock, the reflex arc begins functioningwithout the inhibitory or regulatory impulses from the brain, creating localspasticity and clonus. Initially absent deep tendon reflexes may thereforebecome hyperactive as spinal shock ends. Such spasticity may be useful inincreasing function by, for example, assisting in emptying the bladder andbowel.

FIGURE4-6Sacralsparing.

PrognosticationofAmbulatoryFunctionThoraciclesions,iftheyarecomplete,createsimilarproblemsregardlessofthe

levelofinvolvement.Becausethethoraciccorddoesnotsupplyinnervationtoany extremity, a complete thoracic lesion at any level leaves the patientparaplegic. The major diagnostic consideration in determining the neurologiclevel is that of sensory innervation to the trunk and, to a lesser extent,innervationoftheabdominalmusculature.Inprognosticatingthepatient’sfutureperformance,itisimportanttoassessthefunctionofthesegmentallyinnervatedabdominalandparaspinalmuscles thataid inbalanceforsitting,standing,andwalkingduringrehabilitation.

T1-T8:Ingeneral,aparaplegicwithalesionanywherefromT1toT8canbeindependentinallwheelchairactivities,whereasthemorecomplexmotions,suchasgettingupfromthefloorandcurbjumpingwithawheelchair,aremoredifficultforthosewithlesionsfromT1toT4.

T6:AT6paraplegichascompleteupperextremityandthoracicmusculature,andcanstabilizehimselfagainsthispectoralgirdle.

T9-T12:AparaplegicwithalesionfromT9toT12canwalkindependentlywithlonglegbracesandcrutches.

L1-L3:AparaplegicwithalesionfromL1toL3andpelvicstabilitycanambulatewithlonglegbracesandforearmcrutchesifthepatientwishes.

L4-S2:AparaplegicwithalesionfromL4toS2canexistindependentofhiswheelchairusingshortlegbracesandforearmcrutches.Thepatientiscompletelyindependentinallactivities.

AlthoughparaplegiamayresultfromalesionlocatedanywherefromT1toL1,themostcommonsiteforalesionisbetweenT12andL1.Thefacetjointsbetween T12 and L1 are lumbar in nature and face laterally, whereas thosebetween theother thoracicvertebraeare thoracic innature,and facevertically(Fig. 4-7). Thus, the angle between the facet joints of T12 and L1 is in thesagittalplane,permittingmoreflexionthanthefrontalalignmentofthethoracicjoints.Manyoftheotherthoracicvertebraearefurtherlimitedintheirmotionbythe rib cage. This greater concentration ofmotion at theT12-L1 articulationsleads to a point of stress and a greater potential for fracture and subsequentparaplegia(seeFig.4-15).

Note that there is very little room in the spinal canal at this level; anyvertebraldislocationisalmostcertaintocauseneurologicproblemsasaresultof

directpressureonthecord.Extremeflexionandrotationisthecauseoffracture-dislocationofthethoracicspine,andusuallyleadstoparaplegia.

PrognosticationofBladderandBowelFunctionRestoringusefulfunctiontothebladderandbowelandthusacatheter-freestateis crucial for tetraplegic and paraplegic patients. A bladder that must beregularlyemptiedthroughacatheterispreytorepeatedinfectionsandexcessiveautonomousdysreflexia (resultingfromdistensionof thebladder,amongotherperipheral stimuli) causing paroxysmal hypertension, bradycardia, andnonthermoregulatorysweating.Evaluatingtheextentofsacralsparingmaygivea clue to the possible return of function. Usually, when innervation of thebladderanditscentralmechanismsisintact,voidingfunctionrapidlyreturnstonormal.Iffunctionisonlypartiallydisrupted,aresidualneurogenicdisordercanberestoredtousefulfunctionfairlyquicklybyretraining.

IncompleteLesions:Anincompletelesionmayaffectthebladderandbowelinvariousways.Ifvoluntaryflexionofthegreattoeispresent,perianalsensationisintact,andthereisvoluntarycontractionoftheanalsphinctermuscle,theentiresacralinnervationtothebladderandbowelhasprobablybeensparedandvoluntarybladderandbowelfunctionwillreturn,usuallywithinafewdays(Fig.4-6).

FIGURE4-7Differencesinfacetjointanatomyofthethoracic

andlumbarspines.

Ifperianalsensationisnormalandthereisnovoluntarycontractionoftheanal sphincter, the sacral segmentsmay have suffered partial damage (partialsacralsparing);bladderandbowelfunctionmayundergoonlypartialrecovery.

CompleteLesion:Acompletelesionwithnosacralsparinghasgreatinfluenceonbladderandbowelfunctions.First,voluntaryflexionofthegreattoe,perianalsensation,andvoluntarysphinctercontrolareabsent,indicatingpermanentlossofcentralcontrolofbladderandbowelfunction.Second,theperianalsphincterreflex(analwink)andthebulbocavernosusreflex(inwhichasqueezeoftheglanspenisstimulatesananalsphinctercontraction)(Fig.4-8)maybepresenttoindicatethatreflexinnervationofthebladderandbowelisintact.Thebladdercanbeexpectedtocontractonareflexbasis,andthebowelwillemptyasaresultofareflexinducedbyfecalbulborbyarectalglycerinsuppository.

It is rare that all reflexes remain absent after the initial period of spinalshock,resultinginanatonicbladder,constipation,andileus.Duringtheatonicperiod,thebladdercannotcontractbyreflexactionandmustbecatheterizedoremptied bymanual pressure on the lower abdomen.To empty the bowelwillrequireenemasaswellasmanualevacuationif thestool is inspissated.Astheatonicphasepasses,thebladderbeginstocontractreflexly,andthepatientcanbetrainedtoemptyitusingitsreflexaction.

FIGURE4-8Thebulbocavernosusreflex.

HerniatedThoracicDisksThethoracicspinehastheadvantageofattachmenttotheribsandsternalplate,whichsplintthevertebraeandprovideaddedstability.Withlessmotion,thereislesschancefordiskherniationandfractureandsubsequentneurologicproblems.Thus, thoracic herniated disks are rare in comparison to cervical and lumbarherniateddisks.

Herniated thoracic disks usually produce cord involvement, whereaslumbar and cervical disks usually produce nerve root involvement. Becausethereislittleextraduralspaceinthethoracicspinalcanal,acomparativelysmalldiskprotrusionmayhavepronouncedeffectson theneurology(Fig.4-9). It ismore difficult tomake a clinical diagnosis of a herniated thoracic disk than aherniated cervical or lumbar disk. Although evaluation of muscle power,reflexes,sensation,andbladderandbowelfunctioncanassistindeterminingthelevelofinvolvement,magneticresonanceimaging(MRI)isthecornerstoneforestablishing the diagnosis. Note that with herniated thoracic disks, paraplegia

occasionallyoccurs.Motor power is impaired, but not in a myotomal or neurologic pattern.

Proximalanddistalmusclegroupsareequallyweak,andlegweaknessmaybeunilateral or bilateral. Weakness of the lower abdominal muscles may beapparent, a situation that can be evaluated by Beevor’s sign (see page 37).Muscleweaknessmayvary frommildparesis to completeparaplegia.Muscletoneisincreasedinmostpatients,asonewouldexpectinanuppermotorneuronlesion.

FIGURE4-9Aherniatedthoracicdisk.

SensationExaminationcandeterminethelevelofsensoryinvolvement.Usually,itisoneortwolevelslowerthanthebonyleveldepictedontheMRI.

ReflexesDeeptendonreflexes:patellarandAchillestendonreflexesareincreased,brisk,orexaggerated.

Superficialreflexes:abdominalandcremastericreflexesareabsent.Pathologicreflexes:Babinski’sandOppenheim’ssignsareusuallypresent

(Figs.4-3and4-4).

BladderandBowelFunctionMostpatientshavenobladderorbowelsymptoms.Occasionally,apatientmayexperienceurinaryretention.

Itshouldbeclearfromthisdiscussionthatthesignsvarydependingontheextent of the herniation. The variations themselves may be a tip-off to thediagnosis.

EvaluationofSpinalStabilitytoPreventFurtherNeurologicLevelInvolvementAfter spinal trauma, it is crucial to determine whether the spine is stable orunstable inorder toprotect thespinalcord. If thespine isunstable, itmustbestabilized immediately to prevent further damage to the cord, and possibletetraplegiaandparaplegia.Thenameofthegameistoprotectthespinalcord.

DiagnosisThediagnosisofanunstablespineisbasedonthehistoryofthemechanismofinjury, the physical examination, and an x-ray examination. Stability dependsessentiallyontheintegrityoftheposteriorligamentouscomplex,whichconsistsofthefollowing:1. Supraspinousligament2. Interspinousligament3. Facetjointcapsule4. Ligamentumflavum(Fig.4-10).

Thebreakdownofthisligamentouscomplexcanbediagnosedbyspecificcriteria,asshowninTable4-1.

X-ray shows instability, showswhether there is separationof the spinous

processes,dislocationofthearticularprocesses,andfracture.Physicalexaminationdetermineswhetherthereisapalpablespinaldefect

(Fig.4-11).Historymayestablishwhethertheinjurywascausedbyflexion-rotationor

excessiveflexion.Directlongitudinalpullrarelyrupturesfibersoftheposteriorligamentouscomplex.However,directlongitudinalpullcombinedwithrotationfrequentlyrupturesfibersandresults inspinal instability.Ligamentoushealingissimplynotstrongenough toensurespinalstability:aspinefusion isalmostalways necessary. If the fracture-dislocation does not disrupt the posteriorligamentouscomplex,bonehealingisusuallystrongenoughtoensurestability.

FlexionInjuryIf,duringflexioninjury,theposteriorligamentandcomplexremainsintact,theforceof flexion is spentonvertebral body, and awedge compression fractureoccurs. The vertebral end plates remain intact, and the spinous processes areonlyminimallyseparated.Awedgecompressionfractureismostoftenseeninthe cervical and lumbar spines, and is considered a stable fracture; the bonefragmentsarefirmlyimpactedandtheposteriorligamentouscomplex,includingtheanteriorandposteriorlongitudinalligaments,remainsintact(Fig.4-12).

Excessive flexion results in tearingof the posterior ligamentous complexanddisengagementoftheposteriorfacetjoints,leadingtopuredislocation.Thespinous processes are separated, and the vertebral bodies remain uncrushedbecausethereisnofulcrumaroundwhichtocompressthem.Thisinjuryismorecommoninthecervicalspinethaninthelumbarspine;itdoesnotoccurinthethoracicspinebecauseofthestabilityofferedbytheribsandsternalplate.Puredislocationssuchastheseareunstable(Fig.4-13,Table4-2).

FIGURE4-10Theposteriorligamentouscomplex.

TABLE4-1CRITERIAFORSTABILITYOFSPINEHISTORYOFMECHANISMOFINJURY

PHYSICALANDNEUROLOGICEXAMINATIONS

X-RAYEXAMINATIONSPECIFICCRITERIA

Flexion-rotationExcessiveflexion

PalpablespinedefectMotor/reflex/sensationalterationAbrasionsontheback

SpinousprocessseparationArticularprocessdislocationand/orfracture

Disruptionofposteriorligamentouscomplex

FIGURE4-11Apalpablespinaldefectindicatinganunstablespinalinjury.

FIGURE4-12Astableflexioninjury.

FIGURE4-13Anunstableflexioninjury.

Flexion-RotationInjuryFlexion-rotation injury results in fracture-dislocationsof the spine (Fig. 4-14).Theposteriorligamentouscomplexruptures,therotatingspinedislocatesatthefacet joints, and the articulating processes fracture. A slice fracturemay alsooccur in the vertebra below the facet dislocation. In addition, the spinousprocessesarepulledapartandlaterallydisplaced(Fig.4-15).Thistypeofinjuryisconsistentlyassociatedwithparaplegia.Injuriesinthethoracolumbararea,itisveryunstableandmustbeprotected,forapartiallesion,orevenacordstilluntouched,canbeconvertedintoacompletelesion(Figs.4-12and4-16,Table4-3).

FIGURE4-14Aflexion-rotationinjuryresultinginafracture-dislocationofthespine.

HyperextensionInjuriesIn hyperextension injuries (to the cervical spine), the anterior longitudinalligamentandannulusaredisruptedandextension-dislocationoccurs.Theinjurybecomesstableif theneckisheldinflexion.Frequently,x-raystakenwiththeneckinflexionarenegative.

CompressionInjuriesIncompressioninjuries,theposteriorligamentouscomplexandtheanteriorandposteriorlongitudinalligamentsremainintact,andthespinousprocessesarenotseparated.Thespineremainsstable.However,afragmentthatburstsposteriorlymaycompressthecordandcausetetraplegiainthecervicalspineandparaplegiainthelumbarspine.

TABLE4-2CRITERIAFORSTABILITYOFCERVICALSPINE

PHYSICALEXAMINATION

HISTORYOFMECHANISM

INTEGRITYOFPOSTERIORLONGITUDINAL

NEUROLOGICFINDINGS

PALPABLESPINEDEFECT X-RAY

OFINJURY STABILITYLIGAMENTCOMPLEX (NF) (PSD) FINDINGSFlexion Stable Intact OccasionalNF PSD Vertebral

bodycrushordislocation

Excessiveflexion

Unstable Notintact OccasionalNF

Extension Stable Intact OccasionalNF None NoneFlexion-rotation Unilateral:

stableBilateral:unstable

Notintact NF PSD Facetdislocation

FIGURE4-15Anatomyofanunstableflexion-rotationinjury.

FIGURE4-16Thoracolumbarfracture-dislocation.

TABLE4-3CRITERIAFORSTABILITYOFTHORACOLUMBARANDLUMBARSPINE

PHYSICALEXAMINATION

INTEGRITYOFTHE PALPABLE

HISTORYOFMECHANISMOFINJURY STABILITY

POSTERIORLIGAMENTCOMPLEX

NEUROLOGICFINDINGS(NF)

SPINEDEFECT(PSD) X-RAYFINDINGS

Flexion Stable Intact None None Wedgevertebrae,minimalseparationofthespinalprocess

Excessiveflexion

Unstable Notintact NF PSD Purevertebralbodydislocation;separationofthespinousprocess

Flexion-rotation*

UnstableMostunstableofallvertebralinjuries

Notintact NF PSD Spinousprocessseparation;articularprocessdislocationandfracture;wedgesliceofthelowervertebra

Compression Stable Intact RareNF None Burstvertebrae;spinousprocessesnotseparated;vertebralbodyisshattered;fragmentmaybedisplaced

Extension Stable Intact;rareinjury(mostcommonincervicalspine)

NF None None

*Mostcommonfractureassociatedwithparaplegia.

Meningomyelocele

DeterminationofLevelDetermining the level of neurologic involvement in meningomyelocele iscrucial.Itpermitstheevaluationofthefollowingfivemajorfunctionalcriteria:1. Determinationoftheextentofmuscularimbalancearoundeachofthemajor

jointsofthelowerextremity2. Evaluationofthedegreeandcharacterofanydeformity3. Assessmentofremainingfunctionandtheneedforbracingorsurgery4. Evaluationofbladderandbowelfunction5. Baselineanalysisforlong-termfollow-up

Althoughthedefectfrequentlycausesa total lossof innervationbelowit,thisisnotalwaysso.Inmanycases,therewillbepartialinnervationofseverallevels below themajor level of involvement, or partial denervation of severallevels above it. It is therefore necessary to determine not only the level thatseemstobeprimarilyinvolvedbutalsotheextenttowhichotherlevelsmaybeaffected.The level of involvement can be determined throughmuscle testing,sensory testing, reflex testing, examination of the anus, and evaluation ofbladderfunction.

Itiseasiertotestanewborninfantthanachild.Intheinfant,theskincanbe pinched to provide a painful stimulus and themuscle being tested can bepalpated for contraction: the muscle will either react (positive indication ofmuscle function) or will remain inactive (indication of no muscle function).Althoughitisdifficulttogrademusclestrengthaccuratelyinaninfant,itwillbeevident frompalpationandobservationwhether themuscle is functioningataminimum of grade 3: movement possible against gravity, but not againstresistancebytheexaminer.Theinfant’smuscularfunctioncanalsobetestedbyappropriate electrodiagnostic studies such as electromyography and muscle

stimulationtests.Childrenaremoredifficulttotestbecausetheymayrefusetorespond, forcing the examiner to test many times to obtain an accurateevaluation. Inaddition,musclegrading isanecessityassoonas it ispossible,especiallywhenachildisoldenoughtocooperate,becausethechildmaylosemusclepowerorthecordlevelofinvolvementmayascend,reducingfunctionalcapacity. As a result of such shifting involvement, further evaluation andsurgicalinterventionmaybenecessary.

Deformities that result from meningomyelocele are usually caused bymuscle imbalance. If the muscles around the joint are not working or if allmusclesarefunctioningequallywell,deformitiesseldomdevelop.It isusuallywhenamuscle isworkingeitherunopposedor against aweakenedantagonistthat a deformity occurs. A mild muscle imbalance acting over a prolongedperiod of time may produce a deformity. Development of muscle imbalanceafterbirthasaresultoftheinvolvementofadditionalneurologiclevelsmayalsolead to deformities. Theymay also appear as a result of postural problems ifbracesor splints are incorrectly applied, if the limbs remain constantly inoneposition until they become fixed, or if the patient is allowed to lie in oneposition in the crib (in most instances, the hips flex, abduct, and externallyrotate;thekneesflex;andthefeetmoveintoafewdegreesofequinus).

Once a fixed deformity has developed, it tends to remain, even if themuscular imbalance disappears. For example, if nerve roots higher than theoriginal lesionbecomeinvolved,anexistingdeformitywillusuallynotcorrectitselfeventhoughthepreviouslyunopposedmusclehasceasedtofunction.

Evaluatetheneurologicorcordlevelofinvolvementbymotortestingeachof the joints of the lower extremity. Then review the information within thebroaderconceptsofneurologiclevelstoestablishthediagnosis(Table5-1).

Thefollowingmeningomyeloceleexaminationwillevaluateeachpossiblelevel of involvement from L1-L2 to S2-S3, its functional deficits, and itspotentialforcausingdeformity(Fig.5-1).

L1-L2NeurologicLevel(L1IsIntact,L2IsNot)

MotorFunctionHip

Flexion:absentExtension:absent

Adduction:absentAbduction:absentNofunction;theremaybesomehipflexionfromthepartialinnervationof

theiliopsoas(T12,L1-L3).

TABLE5-1MOTORTESTINGFORNEUROLOGICLEVELJOINT ACTION LEVELHip Flexion

ExtensionAdductionAbduction

T12,L1-L3S1L2-L4L5

Knee ExtensionFlexion

L2-L4L5,S1

Ankle Dorsiflexion(ankleextension)Plantarflexion(ankleflexion)InversionEversion

L4,L5S1,S2L4S1

FIGURE5-1Meningomyelocele.

KneeExtension:absentFlexion:absentNofunction,nodeformity

FootDorsiflexion:absentPlantarflexion:absent

Inversion:absentEversion:absentNo function; if there is any deformity, it may be a result of either the

intrauterine position, a loss of function where there was once a muscleimbalance,oracribpositionthathasproducedhipandkneeflexioncontracturesandequinovarusdeformityofthefoot.Thefootnormallyhasafewdegreesofequinuswhenatrest,apositionthatmaybecomefixed.

SensoryTestingThereisnosensationbelowtheL1band,whichendsapproximatelyone-thirdofthewaydownthethigh(Fig.5-2).

FIGURE5-2Lumbarsensorydermatome.

ReflexTestingNoneofthedeeptendonreflexesofthelowerextremityfunction.Occasionally,reflexactivitymayoccurasaresultofthefunctioningofaportionofthecordbelowtheinvolvedneurologiclevel(intactreflexarc).

BladderandBowelFunctionThe bladder (S2-S4) is nonfunctioning, the patient is incontinent, the anus ispatulous, and the analwink (S3, S4) is absent. It should be noted that sacralsparing is not uncommon at any level. Lesions that give a pattern of

involvementinthesacrallyinnervatedlegmusclesbutadequateinnervationofthesphinctermusclesarealsocommon.

MotorFunctionHip

Flexion:partialExtension:absentAdduction:partialAbduction:absentFlexion is considerable, because the iliopsoas is almost completely

innervated.Thereis,inaddition,ahipflexiondeformitybecausetheiliopsoasisunopposedbythemajorhipextensor,thegluteusmaximus(S1,S2).Thereisasmalldegreeofhipadduction,withacorrespondingslightadductiondeformitybecausetheadductorgroup(L2-L4)ispartiallyinnervatedandisunopposedbythemainhipabductor,thegluteusmedius(L5,S1).

KneeExtension:partialFlexion:absentTheknee isnotdeformed inspiteof thesmallamountof functionof the

kneeextensor,thequadriceps(L2-L4).Thereisnosignificantclinicalfunction.

Foot:Nofunction,nomusculardeformity,exceptasmentionedearlier.

SensoryTestingThere is no sensation below the L2 band, which ends two-thirds of the waydownthethigh.

ReflexTestingNoneofthelowerextremityreflexesarefunctioning.

BladderandBowelFunctionThere is no function of the bladder and bowel. The patient cannot urinate instream; the patient is only able to dribble urine. A streammay appear if the

patient is crying, as a result of the tighteningof the rectus abdominusmuscleandthecorrespondingincreaseinintra-abdominalpressure.

MotorFunction(Fig.5-3)

HipFlexion:presentExtension:absentAdduction:presentAbduction:absentThehiphasflexion,adduction,andlateralrotationdeformities.

FIGURE5-3A,BNeurologiclevelL3-L4:motorfunction.

KneeExtension:presentFlexion:absentThekneeisfixedinextensionbytheunopposedquadriceps.

FootDorsiflexion:absentPlantarflexion:absentInversion:absent

Eversion:absentTherearestillnoactivemusclesinthefoot.

SensationTestingSensationisnormaltotheknee.Belowtheknee,thereisnosensation(Fig.5-4).

FIGURE5-4NeurologiclevelL3-L4:sensation,reflex,andbladderandbowelfunction.

ReflexTestingThere may be a slight, but obviously diminished, patellar reflex (L2-L4),becausethereflexisprimarilyL4.

BladderandBowelFunctionNofunction.

HipFlexion:presentExtension:absentAdduction:presentAbduction:absentThehiphasbothflexionandadductiondeformities,because the iliopsoas

(T12-L3)andadductormuscles(L2-L4)arestillunopposed.Suchanunopposedadduction may over time result in a dislocated hip and, eventually, a fixedflexion-adductiondeformity.Forambulation,fulllegbracingwillbenecessary,includingtheuseofapelvicband,becausethehipisunstablewithoutextensionandabduction.Surgeryisalsoapossiblesolution.

FIGURE5-5A,BNeurologiclevelL4-L5:motorfunction.

KneeExtension:presentFlexion:absentThekneehasanextensiondeformityasaresultoftheunopposedactionof

the quadriceps. Themain knee flexors, themedial and lateral hamstrings (L5and S1), are denervated. An extended knee is relatively stable, and futurebracing is not necessary. However, because the hip must be braced (unlesssurgeryisperformed),thekneeisalsobraced.

FootDorsiflexion:partialPlantarflexion:absentInversion:partialEversion:absentTheonlyfunctioningmuscleinthefootisthetibialisanterior(L4)because

everythingelseisinnervatedbyL5,S1-S3.Theinsertionofthetibialisanterioronthemedialsideofthefootatthefirstmetatarsal–cuneiformjunctioncausesthe foot to be dorsiflexed and inverted. In this position, the foot is bothunbalanced and unstable, and the tibialis anterior may have to be surgicallyreleased. The foot is not plantigrade and is without sensation; thus, skinbreakdownmay occur. Bracing is necessary, but fitting shoes and getting thefootintoabracemaybedifficultifsomecorrectionisnotachieved.

SensoryTestingSensationextendstothemedialsideofthetibiaandfoot.Thelateralaspectofthetibia(L5)andthemiddleandlateralportionsofthedorsumofthefootareanesthetic (Fig. 5-6). A pinprick is the most effective way to test infants forsensation; if there issensation, thechildcriesormoves theextremity.Atripleresponse to thepinprick (flexionof thehipandknee,dorsiflexionof the foot)shouldnotbeconfusedwithmotorfunctionatthesejoints.Suchageneraltriplereflexresponsemayoccurevenifthepatientiscompletelyparalyzed.

ReflexTestingThepatellarreflex(predominantlyL4)functions,whereasthetendonofAchillesreflex(S1)doesnot.IfthereishyperactivityinthetendonofAchillesreflex,aportion of the cord below the original lesion has developedwith intact nerveroots,withoutconnectiontotherestofthecord.Thus,theS1anklereflexarcisintact,andonlytheinhibitoryandcontrollingfactorofthebrainismissing.

FIGURE5-6NeurologiclevelL4-L5:sensation,reflex,andbladderandbowelfunction.

BladderandBowelFunctionNeitherthebladdernorthebowelfunctions.

L5-S1NeurologicLevel(L5IsIntact,S1IsNot)

HipFlexion:presentExtension:absentAdduction:presentAbduction:present

FIGURE5-7A,BNeurologiclevelL5-S1:motorfunction.

Thereisaflexiondeformityofthehip,becausethegluteusmaximusisnot

working.Thereisnowabalancebetweenadductionandabduction;however,aminimal adduction deformity may still exist because the gluteus medius,partiallysuppliedbyS1,isslightlyweak.Becauseofthispartialbalance,thereis usually no hip dislocation. However, if the gluteus medius is excessivelyweak, the hip may later sublux. For ambulation, bracing or surgery will benecessarytopreventseverefixedflexiondeformity.

KneeExtension:presentFlexion:partialThe knee is relatively well balanced, and there are no deformities. The

extensors are working; the flexors are functioning in part, with the medialhamstrings (L5) in and the lateral hamstrings (S1) out. Because of this, theremaybeaslightweaknessinflexion.Bracingwillbeunnecessary.

FootDorsiflexion:presentPlantarflexion:absentInversion:presentEversion:absentThe dorsiflexors all function. Therefore, the foot will have only a

dorsiflexiondeformity(calcanealfoot).

SensoryTestingSensationisabsentonthelateralsideandplantarsurfaceofthefoot(Fig.5-8).Elsewhere,itisnormal.

ReflexTestingThetendonofAchillesreflexisstillabsent.

FIGURE5-8NeurologiclevelL5-S1:sensation,reflex,andbladderandbowelfunction.

BladderandBowelFunctionThebladderandbowelarestillnonfunctional.

S1-S2NeurologicLevel(S1IsIntact,S2IsNot)

HipFlexion:presentExtension:partialAdduction:present

Abduction:presentThehipisalmostnormal;theremaybeslightgluteusmaximusweakness,

whichisinnervatedbyL5,S1,andS2.

KneeExtension:presentFlexion:presentThekneeisnormalandwellbalanced.

FIGURE5-9A,BNeurologiclevelS1-S2:motorfunction.

FootDorsiflexion:presentPlantarflexion:partialInversion:presentEversion:presentThetoesofthefootmaybecomeclawed,becausetheintrinsicmusclesare

still not functioning. In addition, plantar flexion is stillweak.Future gaitwillshow weakened or absent toe-off, and the forefoot may be broken on thehindfootfrommuscleimbalance(calcaneovalgusoftheforefoot).Thefootmayhaveaverticalordislocatedtalus(convexpesvalgus).

SensoryTestingSensationisnormalexceptfortheposteriorstripinthethighandlegandonthesoleofthefoot(S4)(Fig.5-10).

ReflexTestingThetendonofAchillesreflex,althoughitfunctions,maybeslightlyweakened.ThereflexispredominantlyanS1reflexwithelementsofS2.

BladderandBowelFunctionThebladderandbowelarestillnotfunctioning.

S2-S3NeurologicLevel(S2IsIntact,S3IsNot)

MotorFunctionHip:Normal.

Knee:Normal.

Foot:Thetoesofthefootmaybecomeclawedintime;theremayalsobeacavovarusdeformity.

FIGURE5-10NeurologiclevelS1-S2:sensation,reflex,andbladderandbowelfunction.

SensoryTestingSensationisnormal.

ReflexTestingReflexisnormal.

BladderandBowelFunctionThereisoftensomebladderactivity;aportionoftheanalwinkispresent.

MilestonesofDevelopment

Sitting,standing,andwalkingarethreedevelopmentalindicatorsthatareusefulin determining the future grossmotor functional capacity of the patient.Mostpatients with meningomyelocele experience some delay in reaching thesemilestones; the amount of delay and degree of difficulty that they encounterprovidevaluableinformationastothecourseoffuturerehabilitation.

SittingNormally,achild learns tobalancehimselfwhile sittingat sixmonthsofage,andcanpullhimselftoasittingpositionatseventoeightmonths.Achildwithalesion above L3 sits late—at approximately ten months—because of muscleweaknessaroundthehips.Achildwithahighthoraciclesionmayhavespinalinstability, forcing him to balance himself, with the help of his hands, in thetripod position. A spinal fusion stabilizes the spine, freeing the hands foractivitiesofdailyliving.

StandingA child is normally able to pull himself to a standing position at nine to tenmonths. A child with a thoracic meningomyelocele is unable to do this, nomatterwhat the level of lesion.He should be offered bracing for stability; hemay still experience some difficulty, however, because braces are both heavyandcumbersome.

WalkingAmbulation normally begins at 12 to 15 months (range; 8 to 18 months).Although almost all children with meningomyelocele have problems withambulation, independent ambulationwith the aid of appliances is possible forthose with normal intelligence and involvement in the lumbosacral region.Childrenareusuallymoreextensivelybracedthantheywouldbeasadultsuntiltheyreachmidadolescence(12to15years).Afterthattime,mostpatientswithlesionshigherthanS1willbecomelimitedambulatorsbecauseoftheexcessiveenergy thatmust be expended as a result of theweight their armsmust bear;ambulationwithbracesandcrutchesrequiresasmuchenergyasrunningattopspeed.

UnilateralLesionsBifidcordswithwidelydiscrepantlevelsoffunctionarenotuncommon.Thereisaseriouspossibilitythatabonyorcartilaginousspurwillcausetetheringofthecordasthecolumngrows(diastomatomyelia)(Fig.5-11);anysignofsuchunilaterallossoffunctionisanindicationforamyelogram.Scoliosis,thelateralcurvature of the spine, is a significant concomitant problem for those in thisgroup.

HydrocephalusFrom 50 to 70 percent of children with meningomyelocele develophydrocephalus, an abnormal increase in the ventricular size, resulting inenlargement of the head and abnormal prominence of the forehead.Hydrocephalus usually develops secondary to Arnold-Chiari malformation(caudal displacement of the brain stem). If it is left unattended, it can lead tospasticity thatmay further decrease already compromisedmuscle function oneither marginally or normally innervatedmuscles. If hydrocephalus is treatedearly, ventricular size, and thereby head circumference, can be maintainedwithin normal limits. The usual method of therapy is with a shunt andappropriaterevisions,ifnecessary.Theshuntisatubethatdrainsexcessspinalfluidfromtheventriclesofthebraintotheperitonealcavityorheart.

FIGURE5-11Diastomatomyelia(Hoppenfeld,S.:JBoneJointSurg.,493:276,1967).

ExaminationoftheUpperExtremityAlthough the great majority of meningomyelocele lesions occur in thelumbosacralregion,higherlesionsaffectingthefunctionoftheupperextremitymay occur in association with these lower lesions, necessitating a completeneurologicevaluationoftheupperextremity.Hydromyelia(enlargementofthecentral canal of the spinal cord) and syringomyelia (liquid filling abnormalcavitiesinthesubstanceofthespinalcord)ofthecervicalcordmayalsooccurin associationwithmeningomyelocele of the lumbar and sacral regions. Boththesepathologiesareprogressiveandrequirecarefulmotorandsensorytestingof the upper extremity with provisions for follow-up care. To patients with

meningomyelocele, theupperextremitiesareparticularly importantbecauseoftheiruseincrutchwalking.

SuggestionsforExaminationofthePatientwithMeningomyelocele1. Do not mistake the withdrawal response for voluntary control of motor

power.Eventhoughapinprickstimulusmaycausewithdrawalatthreejoints—hipflexion,kneeflexion,andankledorsiflexion(thetripleresponse)—theinfantdoesnotnecessarilyfeelthenoxiousstimulus.Itisnecessarytowatchthe child for signs of crying and changes in facial expression to determinewhetherthereexistsacentralrecognitionofpain.

2. Tomuscletestthehamstrings,positionthepatientfacedownontheedgeoftheexaminingtablesothatthehipsandlowerextremitieshangfreely(Fig.5-12).Stabilizehim.Thendeterminewhetherhecanflexhisknees.Ifthekneeflexes, it is working against gravity and is actingwith at least grade threestrength(Fig.5-13).Duringtesting,palpatemediallytodetermineactivityofthe semimembranosus and semitendinosus (L5) and laterally for the bicepsfemoris(S1).

3. Tomuscletestthegluteusmaximus,continuetoholdthepatientinthesameposition and have the patient extend the hips, indicating gluteus maximusactivity(S1)(Fig.5-14).

4. Itisbyfareasiertoevaluatefunctioninyoungchildrenbyplayingwiththemthanbyconductingaformalexamination.

5. Make certain that the patient is warm and comfortable during theexamination.

6. Have the nursing staff record their observations of any spontaneousmovementsofthepatient’sextremities.

FIGURE5-12Positionfortestingthehamstringandgluteusmaximusmuscles.

FIGURE5-13ContractionofthemedialhamstringmuscleindicatesintegrityofL5neurologiclevel;contractionofthelateralhamstringmuscleindicatesintegrityofS1neurologiclevel.

FIGURE5-14ContractionofthegluteusmaximusindicatesintegrityofS1neurologiclevel.

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Note:Pagenumbersfollowedby“f”and“t”refertofiguresandtables.

AAbductionfinger,21–23,22f,23fshoulder,10f

Abductordigitiquinti,21Achillestendonreflex,52testing,54f

Activitiesofdailyliving,cervicalcordlesions,76–78,79fAdductionfinger,23,22f,23fhip,41,41f,42f

Adductorbrevis,41fAdductorlongus,41fAdductormagnus,41fAmbulatoryfunction,prognosticationof,86–87,87fAnnulusfibrosisanterior,27fposterior,27f

Anteriorhorncellloss,andclinicalmuscleweakness,62fAvulsions,nerveroot,33,36,36fAxillarynerve,8,8–10f

BBabinski’ssign,84,84fBeevor’ssign,37,37fBicepsmuscletesting,8–9,11freflextesting,9–10,12f

sensationtesting,13Bilateralfacetdislocationofthecervicalspine,75–76,78f,79fBladderfunctionL1neurologiclevel,82L1-L2neurologiclevel,95L2neurologiclevel,82L2-L3neurologiclevel,96L3neurologiclevel,82L3-L4neurologiclevel,97,97fL4neurologiclevel,83L4-L5neurologiclevel,99f,100L5neurologiclevel,83L5-S1neurologiclevel,101f,102prognosticationof,87–88S1neurologiclevel,84S1-S2neurologiclevel,103,103fS2-S3neurologiclevel,104

BowelfunctionL1neurologiclevel,82L1-L2neurologiclevel,95L2neurologiclevel,82L2-L3neurologiclevel,96L3neurologiclevel,82L3-L4neurologiclevel,97,97fL4neurologiclevel,83L4-L5neurologiclevel,99f,100L5neurologiclevel,83L5-S1neurologiclevel,101f,102prognosticationof,87–88S1neurologiclevel,84S1-S2neurologiclevel,103,103fS2-S3neurologiclevel,104

Brachioradialisreflextesting,14,16fBulbocavernosusreflex,88f

CC1fracture,74,74f

C2fracture,74,75fC3-C7fractures,75–76,76–79fC3neurologiclevel,tetraplegia,67–68,68fC4neurologiclevel,tetraplegia,68–69,69fC5neurologicleveltetraplegia,69–70,70fupperextremitynerverootlesions,7–11,8–12f

C6neurologicleveltetraplegia,70–71,71fupperextremitynerverootlesions,11–15,13–16f

C7neurologicleveltetraplegia,71,72fupperextremitynerverootlesions,15–20,16–20f

C8neurologicleveltetraplegia,70–71,73fupperextremitynerverootlesions,20,20–22f

Cervicalcordlesions,65–80C3neurologiclevel,67–68,68fC4neurologiclevel,68–69,69f

C5neurologiclevel,69–70,70fC6neurologiclevel,70–71,71fC7neurologiclevel,71,72fC8neurologiclevel,70–71,73fneurologiclevels,clinicalapplicationsofactivitiesofdailyliving,76–78,79ffracturesanddislocationsofcervicalspine,74–76,74–79fherniatedcervicaldisks,78transversemyelitis,79–80tuberculosisofthespine,79tumorsofthecervicalspine,79

T1neurologiclevel,72–73uppermotorneuronreflexes,73,74f

Cervicaldisks,herniated,25–29,25–34f,34t,78Cervicalspine,7fcervicalnecksprainversus,29–31,35flocatinggeneraltestfor,29

specifictestfor,28,29–34f,34tpain,25–27,28ffracturesof,74–76,74–79fstabilitycriteriafor,91ttopreventfurtherneurologiclevelinvolvement,89–91,90–92f

Cervicalvertebra,anatomyof,35fCompletespinalcordlesions,85effectonbladderandbowelfunction,88

Compressionfractureofcervicalspine,75,76fCompressioninjuries,91Compressiontest,36fCremastericreflex,84–85,85fCrutches,cervicalcordlesions,77–78

DDeepperonealnerve,42,43fDeltoidtesting,8,8–10fDermatomesofthelowerextremity,42f,45f,55fofthetrunk,82f

Diastomatomyelia,104fDisks,herniatedcervical,25–29,25–34f,34t,78lumbar,56–57,56–60f,57tthoracic,88–89,88f

Dislocationsofcervicalspine,74–76,74–79fDorsalinterossei,21

EElbowextensionorflexion,10fElectromyography,93Extensionlag,39,40fExtensorcarpiradialisbrevis,14fExtensorcarpiradialislongus,14fExtensorcarpiulnaris,14fExtensordigitorum,19f

Extensordigitorumbrevis,45–46,46fExtensordigitorumlongus,45–46,46fExtensorhallucislongus,45,46ftesting,47f

Extremitylower,nerverootlesions,37–63L4neurologiclevel,42–44,43–45fL5neurologiclevel,45–47,45–49fneurologiclevels,clinicalapplicationsofherniatedlumbardisks,56–57,56–60f,57therpeszoster,62lowbackderangementversusherniateddisk,58–59poliomyelitis,62–63,62fspondylolysis,59–61,62fspondylolysthesis,59–61,60–62f

S1neurologiclevel,47–54,49–54fS2-S4neurologiclevel,54–56,55fT12-L3neurologiclevel,38–42,38–42fT2-T12neurologiclevel,37–38,37f

upper,nerverootlesions,7–36C5neurologiclevel,7–11,8–12fC6neurologiclevel,11–15,13–16fC7neurologiclevel,15–20,16–20fC8neurologiclevel,20,20–22f

neurologiclevels,clinicalapplicationsofcervicalnecksprainversusherniateddisk,29–31,35fherniatedcervicaldisks,25–29,25–34f,34tnerverootavulsions,33,36,36funcinateprocessesandosteoarthritis,31–33,35–36f

T1neurologiclevel,21–25,22–25f

FFacetjointdislocationofthecervicalspine,75,77f,78fFemoralnerve,39–40,39–40fFingerabduction,21–23,22f,23fadduction,23,22f,23f

extension,16fflexorstesting,20,21fflexsion,16f,18f

Flaccidity,85–86Flexioninjury,89,91stable,90funstable,91f

Flexion-rotationinjury,91,91–92fFlexorcarpiradialis,18fFlexordigitorumsuperficialis,21fFootdorsiflexion,46fFooteversion,49fextensors,muscletestfor,47ffunction,withmeningomyeloceleL1-L2neurologiclevel,94L2-L3neurologiclevel,95L3-L4neurologiclevel,96f,97L4-L5neurologiclevel,98f,99L5-S1neurologiclevel,100f,101S1-S2neurologiclevel,102f,103S2-S3neurologiclevel,103

inversion,43fplantarflexion,51f

Fracturesofcervicalspine,74–76,74–79f

GGastrocnemius,51fGastrocnemius-soleusmuscles,50,51f,52Gluteusmaximus,52,52f,53ftesting,53f,105f

Gluteusmedius,47,48–49f

HHangman’sfracture,75fHerpeszoster,62Hip

adduction,41,41f,42fextension,52fflexion,38ffunction,withmeningomyeloceleL1-L2neurologiclevel,94L2-L3neurologiclevel,95L3-L4neurologiclevel,96–97,96fL4-L5neurologiclevel,97–98,98fL5-S1neurologiclevel,100–101,100fS1-S2neurologiclevel,102,102fS2-S3neurologiclevel,103

Hoffmann’ssign,73,74fHydrocephalus,104–105Hyperextensioninjuries,91ofcervicalspine,75,77f

IIliopsoas,38–39,38finnervationof,83ftesting,39f

Incompletespinalcordlesions,85effectonbladderandbowelfunction,87–88

Inferiorglutealnerve,52,52f,53fIntercostalmuscles,37Interosseidorsales,22f

JJeffersonfracture,74f

KKneeextension,39ffunction,withmeningomyeloceleL1-L2neurologiclevel,94L2-L3neurologiclevel,95L3-L4neurologiclevel,96f,97L4-L5neurologiclevel,98–99,98f

L5-S1neurologiclevel,101,100fS1-S2neurologiclevel,102,102fS2-S3neurologiclevel,103

LL1neurologiclevel,paraplegia,82,83fL1-L2neurologiclevel,meningomyelocele,94–95,95fL2neurologiclevel,paraplegia,82L2-L3neurologiclevel,meningomyelocele,95–96L3neurologiclevel,paraplegia,82L3-L4neurologiclevel,meningomyelocele,96–97,96f,97fL4neurologiclevel,lowerextremitynerverootlesions,42–44,43–45fL4-L5neurologiclevel,meningomyelocele,97–100,98f,99fL4neurologiclevel,paraplegia,82L5neurologiclevellowerextremitynerverootlesions,45–47,45–49fparaplegia,83

L5-S1neurologiclevel,meningomyelocele,100–102,100f,101fLateralarm,sensationtesting,11,12fLateralforearm,sensationtesting,15,16fLongitudinalligamentanterior,27fposterior,27f

Lowbackderangementversusherniateddisk,58–59Lowerextremity,nerverootlesions.SeeExtremity,lower,nerverootlesionsLumbardisks,herniated,56–57,56–60f,57tnerverootimpingement,anatomicbasisfor,57fversuslowbackderangement,58–59

Lumbarspinesfacetjointanatomyof,87fstability,criteriafor,92t

Lumbricals,21f

MMedialantebrachial-cutaneousnerve,20,22fMedialarmtesting,23Medialbrachialcutaneousnervetesting,23

Medialforearmtesting,20,22fMediannervetesting,17–18,18fMeningomyelocele,93–106,94fhydrocephalus,104–105leveldetermination,93–104L1-L2neurologiclevel,94–95,95fL2-L3neurologiclevel,95–96L3-L4neurologiclevel,96–97,96f,97fL4-L5neurologiclevel,97–100,98f,99fL5-S1neurologiclevel,100–102,100f,101fmotortesting,94tS1-S2neurologiclevel,102–103,102f,103fS2-S3neurologiclevel,103–104

milestonesofdevelopment,104patientexamination,suggestionsfor,105–106,105f,106funilaterallesions,104,104fupperextremityexamination,105

Metastatictumors,79MotorfunctionC3neurologiclevel,67–68C4neurologiclevel,69C5neurologiclevel,69–70C6neurologiclevel,70–71C7neurologiclevel,70–71C8neurologiclevel,72L1-L2neurologiclevel,94L2-L3neurologiclevel,95L3-L4neurologiclevel,96–97,96fL4-L5neurologiclevel,97–99,98fL5-S1neurologiclevel,100–101,100fS1-S2neurologiclevel,102–103,102fS2-S3neurologiclevel,103T1neurologiclevel,72–73

Motorpower,23–24MusclefunctionL1neurologiclevel,82L2neurologiclevel,82

L3neurologiclevel,82L4neurologiclevel,82–83L5neurologiclevel,83S1neurologiclevel,84T1-T12neurologiclevel,81

Musclestimulationtests,93MuscletestingC5neurologiclevel,7–9,10f,11fC6neurologiclevel,11–13,13–14f,15fC7neurologiclevel,15–18,16–19fC8neurologiclevel,20,20f,21fL4neurologiclevel,42–43,43fL5neurologiclevel,45–47,45–49fS1neurologiclevel,47,52,49–53fT1neurologiclevel,21–23,22f,23fT12-L3neurologiclevel,38–41,38–42fT2-T12neurologiclevel,37,37f

Musculocutaneousnervetesting,8–9,11fbiceps,13lateralforearm,15,16f

Myelitis,transverse,79–80Myelogram,ofherniatedcervicaldisk,34f

NNerverootavulsions,33,36,36fNerverootlesionslowerextremity.SeeExtremity,lower,nerverootlesionsupperextremity.SeeExtremity,upper,nerverootlesions

Normalsuperficialreflex,84–85

OObturatornerve,41Odontoidfracture,74–75,76fOppenheim’ssign,84,84fOsteoarthritis,ofuncinateprocesses,31–33,35–36f

Painherniatedcervicaldisks,25–27,28fherpeszosterand,62

Palmarinterossei,23Paraplegia,81–84L1neurologiclevel,82,83fL2neurologiclevel,82L3neurologiclevel,82L4neurologiclevel,82L5neurologiclevel,83S1neurologiclevel,84T1-T12neurologiclevel,81

Patellartendonreflex,44,44fPathologicreflexes,84Patient examination for meningomyelocele, suggestions to, 105–106, 105f,106fPeroneusbrevis,47,49,49fPeroneuslongus,47,49,49f,50fPhrenicnerve,7Poliomyelitis,62–63,62f

QQuadriceps,39–40,39–40ftesting,40f

RRadialextensortesting,13,13–14f,15f,16fRadialnervetesting,15–17,17f,18fRectusabdominus,37Rectusfemoris,40fReflexivetestingC3neurologiclevel,68C4neurologiclevel,69C5neurologiclevel,9–10,12f,14–15,70C6neurologiclevel,14–15,16f,18–19,20f,71C8neurologiclevel,72L1neurologiclevel,82

L1-L2neurologiclevel,95L2neurologiclevel,82L2-L3neurologiclevel,96L3neurologiclevel,82L3-L4neurologiclevel,97,97fL4neurologiclevel,44,44f,83L4-L5neurologiclevel,99–100,99fL5neurologiclevel,47,83L5-S1neurologiclevel,101–102,101fS1neurologiclevel,47,52–53,54f,84S1-S2neurologiclevel,103,103fS2-S3neurologiclevel,104S2-S4neurologiclevel,54T1neurologiclevel,73T12-L3neurologiclevel,41

Reflextesting,24Respiration,cervicalcordlesions,76–77

SS1neurologiclevel,paraplegia,84S1-S2neurologiclevel,meningomyelocele,102–103,102f,103fS2-S3neurologiclevel,meningomyelocele,103–104S2-S4neurologiclevel,lowerextremitynerverootlesions,54–56,55fSacralsparing,85,86fSensationtesting,24C3neurologiclevel,68C4neurologiclevel,69C5neurologiclevel,11,12f,70C6neurologiclevel,15,16f,71C7neurologiclevel,20,71C8neurologiclevel,20,22f,72L1neurologiclevel,82L2neurologiclevel,82L3neurologiclevel,82L4neurologiclevel,83L5neurologiclevel,83S1neurologiclevel,84

T1neurologiclevel,23,24f,73T1-T12neurologiclevel,81

Sensorydermatomesofthetrunk,82fSensorytestingL1-L2neurologiclevel,94,95fL2-L3neurologiclevel,95L3-L4neurologiclevel,97,97fL4neurologiclevel,44,45fL4-L5neurologiclevel,99,99fL5neurologiclevel,47L5-S1neurologiclevel,101,101fS1neurologiclevel,54,55fS1-S2neurologiclevel,103,103fS2-S3neurologiclevel,104S2-S4neurologiclevel,54,55fT2-T12neurologiclevel,38T12-L3neurologiclevel,41–42,42f

Shingles,62Sitting,meningomyeloceleand,104Spasticity,85–86Spinalcordlesionsambulatoryfunction,prognosticationof,86–87,87fbladderandbowelfunction,prognosticationof,87–88cervicalspinestability,criteriafor,91tcompleteorincompletelesion,85effectonbladderandbowelfunction,87–88

flaccidity,85–86herniatedthoracicdisks,88–89,88fparaplegia,81–84sacralsparing,85,86fspasticity,85–86spinalstabilityevaluation,topreventfurtherneurologiclevelinvolvement,89–91,90–92fthoracolumbarandlumbarspinestability,criteriafor,92tuppermotorneuronreflexes,84–85

Spinestability,criteriafor,90tSpondylolysis,59–61,62f

Spondylolysthesis,59–61,60–62fSpurlingtest,32–33Standing,meningomyeloceleand,104Superficialperonealnerve,47,49,49f,50fSuperiorglutealnerve,47,48–49fSupraspinatustesting,9f

TT1neurologicleveltetraplegia,72–73upperextremitynerverootlesions,21–25,22–25f

T1-T12neurologiclevellowerextremitynerverootlesions,37–38,37fparaplegia,81

T12-L3neurologiclevel,lowerextremitynerverootlesions,38–42,38–42fTendonreflexAchilles,52–53,54fpatellar,44,44f

Tetraplegia,65–80C3neurologiclevel,67–68,68fC4neurologiclevel,68–69,69fC5neurologiclevel,69–70,70fC6neurologiclevel,70–71,71fC7neurologiclevel,71,72fC8neurologiclevel,70–71,73fneurologiclevels,clinicalapplicationsofactivitiesofdailyliving,76–78,79ffracturesanddislocationsofcervicalspine,74–76,74–79fherniatedcervicaldisks,78transversemyelitis,79–80tuberculosisofthespine,79tumorsofthecervicalspine,79

T1neurologiclevel,72–73uppermotorneuronreflexes,73,74f

Thoracicdisks,herniated,88–89,88fThoracicspines,facetjointanatomyof,87fThoracolumbarfracturedislocation,92f

Thoracolumbarspinestability,criteriafor,92tTibialisanterior,42testing,43f

Tibialnerve,50,51f,52Transversemyelitis,79–80Tricepsbrachii,17fextension,16ftesting,15–17,17f,18f,20f

Tuberculosisofthespine,79Tumorsofthecervicalspine,79

UUlnarnervetesting,17–18,18fUncinateprocesses,osteoarthritisof,31–33,35–36fUnilaterallesions,meningomyelocele,104,104fUpperextremityexamination,formeningomyelocele,105nerverootlesions.SeeExtremity,upper,nerverootlesions

Uppermotorneuronreflexes,73,74fnormalsuperficialreflex,84–85pathologicreflexes,84

VValsalvatest,34fVastusintermedius,40fVastuslateralis,40fVastusmedialis,40f

WWalking,meningomyeloceleand,104Wheelchair,cervicalcordlesions,77Whiplashinjurytocervicalspine,35fWristextension,muscletestfor,15fWristflexion,16f,18f

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