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LOWERBACKPAIN
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HERNIAOFINTERVERTEBRALDISC腰痛和腰椎间盘突出症StructuralsupportandbalanceforuprightpostureFunctionsoftheSpineProtectionSpinalcordandnerverootsFunctionsoftheSpineInternalorgansFlexibilityofmotioninsixdegreesoffreedomFunctionsoftheSpineLeftandRightSideBendingFlexionandExtensionLeftandRightRotationCranial-theheadortowardstheheadCaudal-thetailortowardsthetailAnterior-thefrontsectionortowardsthefrontPosterior-thebacksectionortowardsthebackVentral-thefrontoranteriorsurfaceDorsal-thebackorposteriorsurfaceBasicTerminologyCranialCaudalAnteriorPosteriorDorsalVentralVertebralStructuresPediclenotchesSlightNotchDeepNotchIntervertebralForamenIntervertebralforamenNerverootsexitVertebralStructuresBodyPedicleLaminaSuperiorArticularProcessSpinousProcessTransverseProcessVertebralForamenAnteriorArchVertebralbodyAnterior1/3pediclesVertebralArchesPosteriorArchPosterior2/3pediclesandposteriorelementsArchesformthevertebralforamenVertebralStructuresArticularprocessesSuperiorArticularProcessParsinterarticularisInferiorArticularProcessZygapophysealJoint(FacetJoint)ParsLumbarVertebraeBody-
L1toL5progressiveincreaseinmassPedicles-
longerandwiderthanthoracic;ovalshapedSpinousprocesses-
horizontal,squareshapedTransverseprocesses-
smallerthaninthoracicregionSpinalforamen-largetoallowforcaudaequinaandnerverootsIntervertebralforamen-large,butwithincreasedincidenceofnerverootcompressionIntervertebralDiscVertebralStructuresEndPlateApophysealRingCartilaginousBonyTheFUNCTIONALUNITofthespineComprisedof:TwoadjacentvertebraeIntervertebraldiscConnectingligamentsTwofacetjointsandcapsulesTheMotionSegmentFibrocartilaginousjointofthemotionsegmentMakesup¼thelengthofthespinalcolumnPresentatlevelsC2-C3toL5-S1Allowscompressive,tensile,androtationalmotionLargestavascularstructuresinthebodyIntervertebralDiscIntervertebralDiscAnnulusFibrosusOuterportionofthediscLamellaeGreattensilestrengthMadeupoflamellaeAnnulusFibrosusLayersofcollagenfibersArrangedobliquely30°ReversedcontiguouslayersIntervertebralDiscNucleusPulposusNucleusPulposusInnerstructureGelatinousHighwatercontentResistsaxialforcesIntervertebralDiscLargestavascularstructureBloodsupplybydiffusionthroughendplatesDamagetothebloodsupplyleadstodegradationofthediscAnatomyandDegenerativeChangeTheVertebralBody(VB)KeyRolesCarry80%oftheaxialloadsthroughVBanddiscEndplatesenablenutritiontodiffusetodiscIntervertebralDiscTheIntervertebralDiscHastworolesShockabsorberofaxialforcesPivotpointinmotionsegmentIntervertebralDiscLigamentsLigamentumflavumPosteriorlongitudinalligamentAnteriorlongitudinalligamentSpinalLigamentsBandsorsheetsoftough,fibroustissuethatconnectbones,cartilage,orotherstructuresBecomeactivewhenstressedtomaximumrangeofmotionProtectthejointsfrombeinghyperflexedTheIntervertebralDiscandDegenerativeChangeTwomajorcomponentsofIVDAnnulusfibrosis:thick,fibrous“radialtire”LamellaeNucleuspulposus:ball-likegelTheIntervertebralDisc(IVD)andDegenerativeChangeByage50,95%ofpeopleshowlumbardiscdegenerationNotallhavesymptomsSignificantchangestoIVDare:WaterandproteoglycancontentdecreasesCollagenfibersofAFbecomedistortedTearsmayoccurinthelamellaeResultsin:DisclosesheightandvolumeLosesresistancetoloadingforcesNolongeractsasashockabsorberOverview-cont.ThemotionsegmentisthefunctionalunitofthespineandconsistsofMuscle(activators)Ligaments(passiverestraints)AdjacentvertebralbodiesA3-jointcomplexoftwofacetjointsandadisc(pivots)Degenerationcanbegininoneormoreofthesejoints,butultimatelyallthreewillbeaffectedDegenerativeConditionsProvideanoverviewofdegenerativeconditionsDegenerativeDiseaseSpinalStenosisHerniatedDiscDegenerativeDisease-OverviewLossofnormaltissuestructureandfunctionduetoagingprocessChangesareusuallygradual,traumasometimesacceleratesDegenerativechangesdonotalwaysleadtoclinicalsymptomsWhenchangescausesymptoms(oftenpain),theprocessisreferredtoasosteoarthritisSpondylosisisdegenerativechangesinthespineAnatomyandDegenerativeChangeTheVertebralBody(VB)DegenerativeChangesSclerosis:IncreasedboneformationadjacenttoendplatesReducesnutritiondiffusingtodiscStiffensendplate,andreducesabilitytoabsorbloadsOsteophytes:FormationofsmallbonyspursCanprojectintoneurostructuresFacetJointsandDegenerativeChangeKeyRolesCarry20%ofcompressiveloadsHelpstabilizespineDegenerativeChangesCartilageliningloseswatercontentCartilagewearsawayFacetsoverrideeachotherLeadstoabnormalfunctionofmotionsegmentAnatomyandDegenerativeChangeLigamentsandMusclesLigamentsattachbonetoboneProvidestability,enablenormalmotionDegenerativeChangesPartialruptures,necrosisandcalcificationsNegativelyimpactfunctionofmotionsegmentDegenerativeDiscDiseaseChangesinclude:DisclosesheightandvolumeCompressiveloadstransferawayfromnucleustomarginsSclerosisofendplatereducesdiscnutritionFacetjointswearawaycartilage,begintooverrideMotionsegmentbecomeshypermobileOsteophytesdeveloptoattempttostabilizemotionsegmentOsteophytesmayencroachonneurostructuresSpinalStenosisNarrowingofthespinalcanaland/orlateralforamenthroughwhichthenervestravelThreetypes:Centralstenosis:incentralspinalcanalwherecordorcaudaequinaarelocatedLateralrecessstenosis:inthetractwherenerverootsexitcanalAcquired:inlateralforamenwherenerverootsexittobodyMostfrequentinlowercervicalandlowerlumbarspineHerniatedDiscOftencalled“ruptureddisc”VerycommonpathologyL3-4,L4-5,L5-S1commonlocationsThoughttobeaculminationofacutetraumaticeventstothediscHerniatedDisc:4degrees
Nuclearherniation:nucleusruptures.NodisruptionofouterannularfibersDiscprotrusion:rupturednucleuscausesouterfiberstobulgeNuclearextrusion:Completesplitinannulus.MaterialleaksbutremainsattachedtonucleusSequesterednucleus:LeakedsubstancenolongerattachedtonucleusINTRODUCTIONThebackandlegpainsince-Greeksrecognizedit.InthefifthcenturyADAurelianusclearlydescribedthesymptomsofsciatica.Thesciaticaarosefromeitherhiddencausesorobservablecauses-afall,aviolentblow,pulling,orstraining.
ThemostnotableoftheseistheLasèguesign,orstraight-legraisingtest,describedbyForstin1881butattributedtoLasègue,histeacher.Thistestwasdevisedtodistinguishhipdiseasefromsciatica.产生腰痛的组织-脊神经背根与DRG不同,背根对机械压力不是始终有反应,除非神经根有炎性或处可易惹状态。Howe在被铬肠线结扎神经根后可以引出多次发电的情况,单一压迫刺激即可引Aα、β、d神经纤维放电5-30秒。被刺激的神经根是有鞘神位由可能含有神经末梢。Jang发现了猫的S1背根中有点状直接受刺激区产生腰痛的组织-脊神经背根最有效的机械刺激是轻度牵拉,与临床情况相吻合。有病间盘水平的神经根比邻近正常的神经根更敏感Kuslich在局麻下椎间盘手术中,对有炎症或压迫的神经根压迫特别敏感,压迫它再现坐骨神经痛Smyth用尼龙线绕过受累神经根,轻拉即再现坐骨神经痛的神经源的化学介质损伤和炎症的组织释放的化学介质使神经末梢致敏。这些神经致敏物质包括由C纤维释放出的P物质、11氨基酸神经肽。P物质导致血管扩张,血浆外渗,肥大细胞释放组胺。这些炎性介质的持续释放引起了疼痛。神经源的化学介质虽然原因还不清楚,P物质可能直接作用神经末梢或间接通过血管扩张,释放组胺、血浆外渗起作用。P物质在神经致敏中起重要作用,这有重临床意义,脊柱的运动正常是无痛的,但在炎症条件下引起疼痛腰痛症状持续的原因
非神经源的化学介质在组织损伤中产生的可以激活和致敏神经末梢的化学介质包括:缓激肽、血清素(5-HT)、组织胺、钾离子、前列腺素。已在椎小关节及邻近组织中发现了P物质,使用10-μg即能同时兴奋低痛阈和高痛阈神经纤维,30分钟后这些神经对机械刺激的痛阈明显降低非神经源的化学介质当将角叉菱胶或陶土注入关节后,神经纤维致敏兴奋性增加,1-2mm的各方关节活动即可导致关节支配神经的持续释放冲动电位。最近的研究表现在神经感受器对机械压力敏感的部位,注入角叉菱胶,会导致神经元放电达3小时非神经源的化学介质这些研究的临床意义:如果关节囊、韧带、肌肉受牵拉,例如脊柱滑脱和椎间盘突出症,引起组织损伤会导致持久的伤害性刺激,并可以导致一种循环状态,肌肉痉挛,痛觉过敏,以致持续性疼痛椎间盘及神经根周围的炎症有关椎间盘的神经生理学研究是有限的。Cavanaugh报告了椎间盘受机械刺激时只偶有少量冲动,只有腹侧硬膜受牵拉才有持续冲动。只有电刺激椎间盘和后纵韧带引起A-d纤维冲动,同椎管内注入致痛物质,像组胺作用一样椎间盘及神经根周围的炎症Yamashita报告了椎间盘对机械压力大部分情况是没有反应。椎间盘内只有静止伤害感受器,它只对损伤或炎症产生的致痛电学物质有反应。McCarron向狗硬膜外腔注入自体的髓核,表现出它的致炎作用。Olmarker发现身体髓核在神经组织中产生炎性和退行性改变免疫和炎症反应腰腿痛当中,原因很复杂,椎间盘突出的大小与疼痛程度不一,生化和机械因素交互作用。有很多证据表明髓核有致免疫原性,自体髓核与血液接触,对髓核自身抗体已发现,虽然很多证据表明介导免疫炎性,绝大多数以前的研究都注意到椎间盘退变和疼痛的产生中的免疫现象标志物。Saal证明突出间盘边缘有免疫细胞,发现了T淋巴细胞IL-1、2,据细胞。浸润的不同程度分级与症状相关。反应程度与术前症状时间相关但病人没有全身的自身免疫性疾病表现,疼痛直接原因不清。磷脂酶A2---PLA2在风湿性关节炎、急性胰腺炎、血清单阴性关节炎、脓毒症表现出明显的炎症作用。它在体内的源性:表1PLA2activiyu
PMN~~~~~~~~~~~~~~~~~~~~3,2Platelet~~~~~~~~~~~~~~~~~~1.4
Plasma~~~~~~~~~~~~~~~~0.006Sperm~~~~~~~~~~~~~~~~~~28.0inflammatorysynovialfluid~~12.1herniatedlumbardisc~~~~~1212.0正常椎间盘内PLA2就有致水肿作用PLA2的神经毒性Steroid局部应用非常有效,在没有免疫反应的生化炎症,作为疼痛发生机制的另一个原因髓核有介导炎性的能力,含有高浓度的PLA2。Saal在有腰痛病人病变节段的椎间盘组织内会有不正常高浓度的磷酸激酶A2-PLA2。髓核、PLA2及别的致炎物质作用到椎间盘的伤害感觉受器,它激活痛感纤维的作用比单纯压力更大PLA2进入神经根后→神经水肿,髓鞘轴突损伤,同注射蛇毒PLA2,但作用程度轻,支持了PLA2的神经毒性硬腰外使用自体髓核,发生传导阻滞,神经周围组织炎症。Leakageofnucleuspulposusmaterialtonerveroots,isapathophysiologicmechanisminLBPandsciatica
Incisionoftheanulusfibrosusinducesnerverootmorphologic,vascular,andfunctionalchanges.Anexperimentalstudy.Kayama--Japan:Spine1996Thenerveconductionvelocitywassignificantlylowerintheincisiongroup(1314m/sec)comparedwiththenonincisiongroup(735m/sec).Theobvioussignsofcapillarystasiswithanincreasednumberanddiameteroftheintraneuralcapillariesintheincisiongroup.
Cultured,autologousnucleuspulposuscellsinducefunctionalchangesinspinalnerveroots
Kayama--Sweden:Spine1998Nucleuspulposuscellsandfibroblastswereculturedfor3weeks,andvariouspreparationswereappliedtothecaudaequinain29pigs.After1week,nerveconductionvelocitywasdeterminedbylocalelectricalstimulation.Applicationofnucleuspulposuscellsreproducedthepreviouslyseenreductioninnerveconductionvelocityinduced.腰痛症状持续的原因
椎间盘及神经根周围的炎症Kuslich在144例椎间盘手术中,在病变椎间盘外侧检查刺激或电刺激产生中度疼痛占70%,重度占30%。突出椎间盘或狭窄的椎间只对DRG或突炎神经根的机械压迫是持续的,就能导致持续性疼痛,或DRG或炎性神经根内压增加这种持续性疼痛就会变为进行性加重。Cavanaugh将自体髓核注入DRG引起1-3分钟的神经释放PLA2致痛原因①致炎因素;②直接作用伤害感受器;③磷脂酶本身的直接造成神经损伤。炎症介定导致源发性神经根坏死,体外证实PLA2直接刺激纤维环伤害感受器。这些化学物质可直接刺激纤维环和周围神细胞中的细小的无髓纤维C或Adeltal。致病物质作用后,伤害感受器的痛域下降。(对机械刺激)正常的生理活动就可以导致腰痛、障碍痛、根性痛(在纤维环外1/3后纵韧带).第二部分:腰痛症状持续的原因
椎间盘及神经根周围的炎症临床、组织化学、生理化学、神经组织学研究,髓核含有化学性致炎、神经退变,急性期有神经兴奋的作用。同样化学物质有氢离子、PLA2免疫球蛋白G等,在椎间盘性疼痛中,增加炎性神经根的敏感性起重要作用PhospholipaseA2sensitivityofthedorsalrootanddorsalrootganglion
OzaktayUSA
:Spine1998JunPhospholipaseA2appearedtobeneurotoxicwhendosesrangingfrom100to400Uwereappliedonthemechanicallysensitivesegmentsofthedorsalrootganglia.PLA2dosescomparabletoserumconcentrationsinhumanrheumatoidarthritiswhenappliedtodorsalrootganglia.TheseresultssuggestthatdorsalrootsanddorsalrootganglionmaybeimpairedbyphospholipaseA2,leadingtosciaticaandlowbackpain.脊髓水平
中枢致敏组织损伤可能导致连续的神经冲动至脊髓,这使后角神经元致敏致敏的神经元痛阈下降,对传入冲动的反应增强,对重复刺激的反应也增强,接受刺激的阈值变宽。恶性刺激导致中枢致敏时,有明确证据后角释放了兴奋性胺基酸和神经肽脊髓水平---中枢致敏在中枢致敏状态下,机械刺激的致痛阈值已下降,使很低的机械刺激就可以让后角发出疼痛信号。变宽的接受阈能把损伤处及附近正常组织的传入信号变为疼痛信号向上传递,这就解释了腰疼痛位不清和持久、及牵涉痛的原因脊髓水平---中枢致敏Gilleffe发现了后角单个神经元可接受从各种脊柱组织传入的信号,呈一种高度会聚接收状态。脊髓后角的神经元可以由压迫皮肤、椎小关节、韧带、及肌肉而兴奋,这种高度会聚功能也是腰痛不易定位的原因ChronicCompressionofDorsalRootGanglionProducedbyIntervertebralForamenStenosis
HuSJ-Xi'an,PRChinaPain1998JulAnexperimentalmodelintherat.Asmallstainlesssteelrod(0.5-0.8mmindiameter)wasinsertedintotheL5intervertebralforamenTheseneuronshadagreatlyenhancedsensitivitytomechanicalstimulationoftheinjuredDRGandaprolongedafterdischarge.apersistentheathyperalgesia5-35daysTheexcitatoryresponseswereevokedintheinjured,butnottheuninjured,DRGneurons.EPIDEMIOLOGY-riskfactors
Multiplefactorsaffectthedevelopmentofbackpain.smoking,pro-longeddailydrivingofmotorvehicles,jobsrequiringfrequentrepetitiveliftingofheavyobjectsandtwisting,theuseofjackhammersandmachinetools,andtheoperationofmotorvehicles
episodesofanxietyanddepression.Itismorecommoninmalesthanfemalesandhasamaximalincidenceinthethirdandfourthdecadesoflife.LUMBARDlSCHERNlATIONBackpainmaybecausedbystimulationofthepainfibersintheouterlayersoftheannulusfibrosus.Alternatively,distortionoftheposteriorlongitudinalligament,whichisrichlyinnervatedbypainfibers,mayresultinbackpain.LegpaincanresultfromcompressionofanerverootbyanHNP腰痛可以起自于椎间盘、椎小关节、肌肉的神经末梢。化学炎性介质释放,使正常无痛的运动变为疼痛性的。髓核是强列的神经根和神经末梢致炎和刺激物质椎间盘与神经根的位置、DRG的特殊神经生理特点、神经根和DRG易被压迫而出现坐骨种经痛。系列恶性冲动使后角感觉神经元致敏,导致的慢性疼痛状态CIinicaIPresentationThefollowingareriskfactorsforherniateddiscdiseaseinthelumbarspine:smoking,pro-longeddailydrivingofmotorvehicles,andfrequentrepetitiveliftingofheavyobjectsandtwisting.Itismorecommoninmalesthanfemalesandhasamaximalincidenceinthethirdandfourthdecadesoflife.Theclinicianmustruleoutacompressivelesionofthesciaticnerveperipherallybeforeascribingthepaintoaherniateddisc.Theremaybeahistoryofapreviousinjury.CIinicaIPresentationAsymptom-HNP.Sciaticaispainalongthecourseofthesciaticnerve.Theclassicsymptomislowbackpainwithradiationofseverepaindownthebackofthelegtotheankleandfoot.Itmaybeassociatedwithneurologicalsignssuchasmotorandsensorylossandoccasionallybladderinvolvement.ThelevelsoflumbarHNPThemostcommonlevels-L4--L5andL5--Sl.Forthisreason,radicularsymptomsalmostalwaysrefertosymptomsbelowtheleveloftheknee,intheL5orS1dermatome.Legsymptomscanvaryfromnumbnesstodysesthesiatotruepain.TheherniationoftheL4--L5disccancompresstheS5andThelumbosacraldisccausescompressionoftheS1nerveroot.
SymptomsandsignsofthelumbarspineThereisoftenassociatedspasmofthespinalmuscleswithtendernessoverthelowerlumbarspineonthesideofthelesion.Themuscularspasmmayproduceascoliosis.Limitationoflateralflexionofthelumbarspinetothesamesidewillbemostmarkedwithaprotrusionlateraltothenerveroot,whilelimitationoflateralflexiontotheoppositesidewillbemostmarkedwithaprotrusionmedialtothenerveroot.FocalsignsFocalsignsaredependentonthedistributionoftheaffectednerveroot.WithL4compressionthereisweaknessofquadricepsandtibialisanterior,withsensorychangeoverthemedialaspectoftheshinanddepressionofthekneejerk.L5rootcompressionmaysolelydeclareitselfbyweaknessofextensorhallucislongus.Anysensorychangeisfoundoverthemedialaspectofthedorsumofthefootandthelateralshin.InanSlrootsyndromeweaknesscanoccurinthebuttockmuscles,thehamstringsorthecalfmuscles.Theanklejerkislikelytobedepressedorabsent.Sensorychangeparticularlyoccursoverthelateralaspectofthefootandthecalf.ProtrusionoftheL4/5discItmaycauseL5rootpressurewithpainradiatingdownthelegtothedorsumofthefoot.Theremaybenumbnessontheoutersideofthecalfandmedialtwo-thirdsofthedorsumofthefootwithweaknessofdorsiflexion,particularlyofthefootandtoes.ProtrusionoftheL4/5discProtrusionsattheL4/5levelwillthuscompresstheL5root,whileprotrusionsattheL5/S1levelwillcompressthefirstsacralroot.ProtrusionoftheL5/S1discItwillpressontheS1nerverootandmayleadtopainandnumbnessontheoutersideofthefootandundersideoftheheel.
ProtrusionoftheL5/S1discTheremaybeweaknessofbotheversionandplantarflexionofthefootwithadiminishedorabsentanklejerk.ProtrusionoftheL3/4discItmaycausepressureontheL4nerveroot
mayleadtonumbnessoverthefrontofthekneeandlegwithdiminutionofthekneejerkandweaknessofthekneeextensors.ProtrusionoftheL3/4discFemoralnervetractiontestCentralprotrusionofalowerlumbardiscItcanpressonthecaudaequinaleadtourinaryretention.Onexaminationthereisusuallyperianalnumbnessandapatulousanus.Emergencydecompressionisessentialtoavoidpermanentdamagetosphincterinnervation.CentraldiscprotrusionFollowingacentraldiscprotrusion,whichcanoccurwithoutanantecedenthistoryofbackpain,caudaequinacompressionoccurs,ofteninanabruptfashion.Severepainresults,withparavertebrallocalizationorwithradiationintobothlowerlimbs.Typically,thereisseveredistallowerlimbweaknesswithfootdrop,depressionoftheanklereflexesandimpairedsphincterfunction.Saddleanaesthesiaiscommon.
中央型Occasionallytheprotrusioniscentral,pressingonthecaudaequinaandaffectingautonomiccontrolofthebladderleadingtourinaryretention.Urgentsurgicaldecompressionofthecaudaequinaisrequiredasanemergency.CIinicaIPresentationAnymaneuverthatincreasesintraspinalpressure,suchasstrainingatstool,coughing,orsneezing,mayexacerbatesymptoms.InoverhalfthepatientswithsciaticafromanHNP,aspecificnerverootcanbeidentified,simplybyhistory.Weakness:
thetibialisanterior---godownstairs,thegastrocnemiussoleusmusclegroup---goingupstairsdifficult.临床表现
流行病学常见于20~50岁患者男女比4~6:1多有弯腰劳动或长期坐位工作史症状腰痛坐骨神经痛马尾神经受压体征腰椎侧突腰部活动受限压痛及骶棘肌痉挛直腿抬高试验及加强实验神经系统表现TreatmentNotallpatientssufferpainAsouterdiscdistorts,mayprotrudeintospinalcanalMayleadtosciatica(paindownbackofleg)Oftenstartwithconservative,non-operativecareSpontaneousresolutionofsciaticaoftenoccursPatientswithcaudaequinasyndromerequiresurgicalattentionCommonsurgicalproceduresinclude:Laminectomy,discectomy,microdiscectomy,endoscopicdiscectomy,ablationprocedurePhysicalExaminationTheposture:OftenthereisafunctionalscoliosisRangeofmotionofthelumbarspinemaybelimitedduetoparavertebralmusclespasmorguarding.Forwardflexionmayincreasethesymptomsofsciatica.Palpationmayshowtendernessinthesciaticnotchduetoirritationofthenerve.PhysicalExaminationStraight-legraisingisperformedbygentlyelevatingtheoutstretchedlegfromthehorizontalwiththepatientlyingsupine.Thedegreeofmovementisrecorded.Themostspecificsignforlumbardischerniationisacontralaterallypositivestraightlegraisingexamination,alsocalledcross-legtest.AfemoralstretchtestusuallyindicatesadischerniationattheL3--L4levelorabove.Ameticulousneurologicexaminationisnecessarytodetectmotorweakness,sensorychanges,anddeeptendonreflexasymmetry.PlainX-raysPlainX-raysareofverylimitedvalueintheinvestigationofalumbarradiculopathy.BesideMarkedfocaldiscspacenarrowing,plainX-raysareoftennormal.Butitsmostimportantvalueisruleoutthebonydisordersofthelumbarspine,TB,Tumor.MyelographyPurpose:ShowcompressionordisplacementofneuralelementsMethod:RadiopaquematerialinjectedintothethecalsacStandardx-raysand/orfluoroscopyReading:NeuralstructuresaredarkContrastmaterialwhiteSpecialRadiographicStudiesSpecialRadiographicStudiesDiscographyPurpose:EvaluatepatencyofdiscEstablishwhetherdisciscausingback/radicularpainMethod:PlaceneedleintodiscunderfluoroInjectdyeintothediscReading:Dyeleaksoutofnucleus=incompetentdiscInjectionreproducespain=discassourceofpain(Provocativediscogram)SpecialRadiographicStudiesComputedTomography(CT/CAT)Purpose:DetectbonytissuepathologiesMethod:Multipleslicesofaxialx-rayimages(1-4mm)ComputerconstructsintopermanentimageHighradiationexposureSpecialRadiographicStudiesMagneticResonanceImaging(MRI)Purpose:DetectsofttissuepathologiesMethod:UsesmagneticandradiowaveenergyShowsatwo-dimensionalsliceCoronal,sagittaloraxialviewNoradiationSpecialRadiographicStudiesBoneScanPurpose:Detectinflammation,infection,tumorMethod:InjectradioisotopeintothebloodstreamIsotopeabsorbedbybonetissueGammascandetectsradiationReading:Darkareas=increasedactivity (hotspot)RadiologyOverviewPlainCTCTisrecommendedastheinitialinvestigationfortheevaluationoflumbardiscdisease,Itcanshowmanydisordersofthelevel:
lumbarcanalstenosisthelateralrecesssyndromecalcificationofthedisc.双侧根管狭窄,椎管狭窄严重
解剖结构变化CTmyelographyCTmyelographycomplementsmyelographyintheinvestigationofsuspectedlumbardiscprotrusion.Myelographyachievesa60-80percentaccuracyinthediagnosisofherniatedlumbardisc.Ittendstofailinthesituationoflateraldiscruptureorwherethereisalargeepiduralspaceorashortduralsac.FormanypatientsplainCTsufficesasaprimaryprocedure.Ifitfails,routinemyelographycanbeconsideredaugmented,insomecases,byCTmyelography.Eithertechniquecanclearlydemonstrateeitheraposterolateral(Fig13.16)orcentraldiscprolapse.MRIMRIisnowthescreeningtechniqueofchoicefortheaccuratedefinitionoflumbardischerniation.UsingT2-weightedimages,thenucleuspulposusandannulusfibrosuscanbedistinguished.SagittalimagingusingbothTlandT2sequencesdefinesthedegreeofdiscprotrusionandtheextentofanyspinalstenosis.MRIAxialviewsaremorevaluableinassessingnerverootcompression.Evenintheabsenceofdiscprotrusion,MRIcanidentifytearsintheannulusfibrosuswhichsometimesenhancewithgadolinium.诊断根据病史、症状、体征及X线平片可作出初步诊断结合CT、MRI,能更准确作出病变间隙、突出方向、突出物大小、神经受压情况及主要引起症状部位的诊断与腰腿痛的其他疾病鉴别ThedifferentialdiagnosisThedifferentialdiagnosisoflumbarneurologicalcompressionincludesthevariouscausesoflowbackpainThecausesoflocalisednerverootpressure.Theseincludesecondarytumoursandmultiplemyelomaofthelumbarspinewhichusuallycausevertebraldestructionwithsparingofthediscs.Fracturesandinfectionsofthespinemayalsocausenerverootandspinalcordcompression.BackPain-SummaryofCausesinthelumbarspineandpelvisTRACTIONInthecaseofsciaticirritationduetoaprolapseddisc,pelvictraction,willhelptodistractthelumbarvertebraeandincreasethesizeoftheintervertebralforamina,thusrelievingthepressureonthenerve.Itmaybenecessarytocontinuethisfortwoorthreeweeks,andthepatientshouldbegraduallymobilisedwithalumbosacralbrace.Occasionallyanepiduralinjectionoflocalanaestheticandsteroidswillalleviatethesymptoms.Inover90%ofcases,conservativemanagementissuccessfulandoperationcanbeavoided.Itisessential,however,thatpatientsbuildupweakextensormusclesofthespineandregularlyexercisethespine.Swimminginawarmpoolisprobablythebestformofexercise.治疗非手术治疗适应症
年轻、初次发作者病程短者休息后症状可自行缓解者X线检查无椎管狭窄方法绝对卧床休息持续牵引理疗、推拿、按摩皮质激素硬膜外注射髓核化学溶解法手术治疗SurgicalinterventionThekeytogoodresultsindiscsurgeryisappropriatepatientselectionandelective.Theunilaterallegpainextendingbelowthekneehasbeenpresentforatleast6weeks.Thisshouldallowathoroughevaluationtoconfirmthediagnosis,levelofinvolvement,andthephysicalandpsychologicalstatusofpatient.Frequentlywhenthereisarushtotheoperatingroomtorelievepainwithoutproperinvestigationboththepatientandphysicianlaterregretthedecision.LumbarlaminectomyIndicationsforoperationonprolapseddiscsNoimprovementinthesymptomsandsignsafter6weeksrest.Anincreaseintheneurologicaldeficit.Bladderorbowelinvolvementsuggestingacaudaequinesyndrome.Itismandatoryandurgentonlyincaudaequinasyndromewithsignificantneurologicaldeficit,especiallybowelorbladderdisturbance.Intractablepain.Thepainshouldhavebeendecreasedbyrest,antiinflammatorymedication,recurringaftertheconservativecare.Theprogressiveorunresponsivelesionswithappreciableneurologicalsignsdespiteconservativemanagement.LumbarlaminectomyorlaminotomyForthepast60years,patientssufferingfromdischerniationunderwenttwoprocedures.Thislaminotomyprocedurerequiresmakingatwo-tofour-inchincisionintheskin,cuttingmuscleandremovingtheboneoverlyingthedamageddisc.Becauselaminotomyissoinvasive,itiscalledan"open"procedure.SpinalstenosisThoughinmanypatientsspinalstenosisiscongenital,inothersitissecondarytohypertrophyofthebonyelementsofthelumbarcanal,ligamentalhypertrophyordiscdegeneration.Thestenosismayprincipallyaffectthecentralcanal,thelateralrecess,ortheintervertebralforamenandnerverootcanalCanalstenosisusuallyaffectsmiddle-agedmen.Typically,paroxysmalnumbnessorparaesthesiae,ratherthanpain,appearinthelowerlimbsduringwalkingandsometimesincertainstandingpostures.Thesymptomsoftenspread,usuallyfromthedistalpartsoftheextremitiestotheproximal,thenresolveafterrestingorlyingflatforseveralminutes.Physicalexaminationtendstobeunrewarding.SpinalstenosisPlainX-raysareoflimitedvalueintheinvestigationofthestenoticsyndromes.High-resolutionCTistheinvestigationofchoice,allowingdefinitionbothofthecentralcanalandofthelateralrecess.Findingsincludeacongenitallynarrowcanal,facetjointdegeneration,hypertrophyoftheligamentumflavumanddegenerativediscdisease.CTmyelographyisseldomnecessary.MRI,thoughfailingtoprovidethesamebonydetailasCT,isatleastitsequalinevaluatingthevariousformsofspinalstenosis.Rarely,aclinicalsyndromesuggestingneurogenicclaudicationisencounteredinpatientswithseverestenosisoftheterminalaorta.SpinalstenosisSpinalorforaminalstenosisismanagedsurgicallyifthesymptomsaredisabling.Lumbardiscprolapse,ifcentral,ismanagedbyimmediatesurgery.Posterolateraldiscprolapseismanagedconservativelyinitiallybutbysurgeryifsymptomsfailtoresolvewithrestorre
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