脊髓損傷的治療BalanceVSImbalance……修復(fù)損傷TofindthebalanceofinjuryandrepairSpinalcordinjury(SCI)isadiseasethatharmfultopeople,trafficaccidentsandfallingetc.causemanySCI.①、原發(fā)性損傷：由于機(jī)械壓迫、出血所致。主要依靠外科手術(shù)。SCIdisorderofmotor,perceptionabsolutelyorpartlyafterexogenicattack

②、繼發(fā)性損傷：由于水腫、炎癥反應(yīng)、局部缺血、脂質(zhì)過(guò)氧化、鈣離子超載所致。主要治療方法有藥物治療、高壓氧治療、電刺激治療、基因治療。原發(fā)性脊髓損傷繼發(fā)性脊髓損傷Medications1.CorticoidsE.g.methylprednisolone,MP2.GangliosiesE.g.GM一13.Neurotrophicfactor,NTFE.g.nervegrowthfactor,NGF4.Scopolamine5.NeuroprotectiveagentsE.g.ionchannelblockers,plateletactivatefactor(PAF)antagonists,glutamatereceptors(GluRs),nitricoxidesynthase(NOS)inhibitors2.Gangliosides:getthoughBBB,highaffinitytotheinjurednervetissueProtectthestructureandfunctionofmembraneHelpNTF,providethesuitedenvironmentReducethetoxicityofGlu,regulatetheactivityofPKCLowertheexcessiveNOandWalleriandegenerationPromotehyperplasiaofaxonImprovetheadministrationwayFindbetterderivantsGM—1+-Shorthalf-lifeCan’tcrossBBBBadeffectofperipheraladministrationCavityformingbylocalperfusionExogenousinfection-HBO

（highpressureoxygen）akindofphysicaltherapy，isplacedinthecabinpressure,patientsintheairthanundertheenvironmentofhighpressureinhaledpureoxygen,thedissolutionofoxygenbyincreasingbloodtoimprovesymptomsandtreatmentofdiseasespurpose.1.Pressureeffect2.Vasoconstriction&anti-coagulant3.anti-bacteriummechanismVolumeofbubblesScopeofobstructionO2contentincreaseα2-Rbrainedema&edemacausedbypressedthebloodflowdecrease,butoxygencontentincreaseaerobes&AnaerobicbacteriaTissueedemaandbleeding,1-2hbegan,6-8hthemostTest:0.2mPaO215%ImprovehypoxiastateHBOindications①acuteinjurycasuedbywound②treattargetedinjury:notseasonabletreatment&Inappropriatehandling

oppressionmyelopathictypecervicalvertebradisease.

③thosewithoperationindicationsadvancesurgicaltreatment.

④ifinjurycompletely,HBOisunefficient.Ifit’spartially,HBOismoreorlessefficient.⑤thesooner,thebetter.在脊髓損傷早期實(shí)施干預(yù)治療，減輕繼發(fā)性損傷程度，盡可能地保護(hù)殘存神經(jīng)束路的功能，改善損傷的微環(huán)境，促進(jìn)神經(jīng)元的軸突再生．成為研究脊髓損傷治療策略中首要的關(guān)鍵環(huán)節(jié)。脊髓損傷后3，7，14NF和GAP43雙標(biāo)染色結(jié)果顯示：對(duì)照組空洞內(nèi)區(qū)域NF呈短棒狀稀疏分布，GAP43分布區(qū)域與NF無(wú)明顯一致性，且表達(dá)較弱；照射組空洞內(nèi)區(qū)域可見(jiàn)NF及GAP43均呈明顯細(xì)長(zhǎng)的神經(jīng)纖維絲狀密布表達(dá)，表達(dá)分布區(qū)域基本一致，部分神經(jīng)纖維樣結(jié)構(gòu)穿越空洞區(qū)域正常成年雄性SD大鼠30只，體重200～250g，星形膠質(zhì)細(xì)胞標(biāo)記物神經(jīng)膠質(zhì)酸性組蛋白(GFAP)抗體，生長(zhǎng)相關(guān)蛋白標(biāo)記物神經(jīng)生長(zhǎng)相關(guān)蛋白(GAP43)抗體，神經(jīng)纖維絲標(biāo)記物神經(jīng)微絲蛋白(NF)及硫酸軟骨素(CS)蛋白多糖標(biāo)記物CS-56抗體，熒光二抗Alexa488標(biāo)記的羊抗兔IgG和TexasRed標(biāo)記的羊抗鼠IgG大鼠急性皮質(zhì)脊髓背側(cè)束全橫斷后，48h內(nèi)為出血期；3～7d為急性期，出血逐漸吸收，同時(shí)以損傷處為中心，灰質(zhì)大部分崩解，殘存部分白質(zhì)開(kāi)始形成空洞及瘢痕組織，但與周圍分界尚不清楚；14dU寸出血已經(jīng)基本吸收，周圍殘存白質(zhì)進(jìn)一步減少，空洞及瘢痕組織明顯形成。結(jié)果顯示各時(shí)間點(diǎn)上，照射組空洞及瘢痕面積均小于對(duì)照組，F(xiàn)igure2HumanGDAgraftsurvivalandsupportofaxongrowthwithinspinalcordDLFinjuries.Injury:Immuno-stainingforhumanmitochondrialmarker(redchannel)免疫組化線粒體標(biāo)識(shí)紅染

higherdensityofaxonswithinhGDAsBMPtreatedinjurysites(A,E)comparedtohGDAsCNTFtreatedinjurysites(B,F)MigrationofhGDAsinw