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首页 癫痫放电的产生

癫痫放电的产生.doc

癫痫放电的产生

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2019-06-12 0人阅读 举报 0 0 暂无简介

简介:本文档为《癫痫放电的产生doc》,可适用于医药卫生领域

癫痫放电的产生Epilepticdischargegeneration癫痫主要是由神经元异常放电所导致的大脑短暂性功能障碍,是一种慢性神经系统疾病,长期困扰着患者,给患者带来了很大的伤害,给整个家庭也带来了很多的烦恼,那么癫痫放电是怎样产生的呢很多人对这个问题都不太了解,为了让给多的人对癫痫疾病有一个深入的了解,下面就请相关癫痫治疗专家给大家介绍一下与癫痫放电的产生相关的知识,希望能够对大家有所帮助。Epilepsyiscausedbyabnormaldischargeofneuronsinthebrainoftransientdysfunction,isachronicdiseaseofthenervoussystem,longtroubledpatients,patientscausedgreatdamagetothewholefamily,alsobroughtalotoftrouble,soepilepticdischargesishowariseManypeopleonthisproblemarenotveryfamiliarwith,inordertogivemorepeopleonepilepticdisordershaveadeeperunderstanding,nowpleaserelatedepilepsyexpertstointroduceandepilepticdischargeshaverelevantknowledge,Ihopeeveryonecanhelp()痛波形成:癫痫起步神经元的单个动作电位并不足以引发脑电图上癫痫放电或癫痫发作,但将这种增强的神经元活动通过相应的轴突联系,在多种促同步化因子,如电压门控离子通道电导异常、细胞膜静息电位稳定性降低、细胞内外离子分布异常、突触兴奋性增加而抑制性减弱等的作用下,经局部反复兴奋环路的增益作用转变成高度同步化的动作电位暴发时就可形成一个大的去极化电位,叫阵发性去极化漂移,此时神经元外钾离子增多,钙离子减少,并可在脑电图上见到不伴有临床发作的间歇期癫痫放电。在对皮质锥体细胞和海马细胞离体或活体研究中发现,间歇期病样放电都伴有阵发性去极化漂移,在海马CA区锥体细胞或一层皮质连接处的锥体细胞间很容易发现这种电位,因而认为其代表神经元的痛性活动,是神经元痛性活动的主要表现。()painwaveformation:epilepsystartedneuronstosingleactionpotentialsarenotsufficienttotriggertheEEGofepilepticdischargesorepilepticseizures,butwillthisenhancedneuronalactivityviathecorrespondingaxonalcontact,inavarietyofsynchronizationfactor,suchasthevoltagegatedionchannelconductanceanomalies,therestingmembranepotential,cellandreducethestabilityofiondistributionabnormalexcitability,synapticinhibitionincreaseswithdecreasedundertheactionofthelocal,recurrentexcitatoryloopgainintohighlysynchronizedactionpotentialsincanformagiantdepolarizingpotentials,calledaparoxysmaldepolarizingshift,theneuronsextracellularpotassiumionsincreased,calciumionsdecreased,andinEEGtoseewithoutclinicalseizuresinterictalepilepticdischargesIncorticalpyramidalcellsandhippocampalcellsinvitroorinvivostudyfound,intermittentperiodsofdiseaselikedischargeisaccompaniedbyparoxysmaldepolarizingshift,inhippocampalCApyramidalcellsorlayercorticalconnectionsamongpyramidalcellswereeasilydetectedbythispotential,sothatitrepresentedneuronspainofsexualactivity,neuronspainactivitymainly动物模型研究资料表明这种放电来自兴奋性突触后电位,并被内源性电压依赖型膜电位所增强,这种增强开始于神经元的除极,当刺激达到激活慢失活钠离子电流阂值时,钠离子内流,增加去极化,随去极化的发生,低阔值的钙电流被激活,进一步增强神经元除极。同时,兴奋性氨基酸介导的兴奋性突触作用增加,最后,高阂值的钠离子、钙离子电流被激活,出现伴有暴发性动作电位的神经元放电。Animalmodelresearchdatashowthatthedischargefromexcitatorypostsynapticpotentials,andendogenousvoltagedependentmembranepotentialsareenhanced,thisenhancedbeganinneuronaldepolarization,whenthestimulustoactivatetheslowlyinactivatingsodiumcurrentthreshold,inwardsodiumcurrent,increaseddepolarization,withdepolarizationoccurs,lowwidthvaluecalciumcurrentisactivated,furtherenhancementofneuronaldepolarizationAtthesametime,excitatoryaminoacidsmediateexcitatorysynapticeffectsincreased,finally,highthresholdofsodiumion,calciumioncurrentisactivated,appearedwithfulminantactionpotentialdischargeofneurons要使在正常情况下很小的兴奋性突触后电位转变成巨大电位必须使其强化,目前已经发现至少有种机制可使病灶内兴奋性突触后电位增强:①抑制减弱②兴奋性超常③高频兴奋性电位:④镁离子介导的电压依赖型受体抑制减弱导致的兴奋性氨基酸受体活动的增加⑤导致癫痫放电的其他神经递质释放增加,同时,中枢内存在的一些内源性电压依赖型电流还可直接增加兴奋性突触的除极效能,包括慢失活的钠离子、钙离子电流和可能代表钙依赖动作电位大而短暂的钙电流。这些机制的共同作用促成了弱小的兴奋性突触电流向巨大的痛性突触后电位的转化。Tomakethenormallyverysmallexcitatorypostsynapticpotentialsintohugepotentialsmustbestrengthened,atpresenthasbeenfoundatleastmechanismsmaycauselesionswithintheexcitatorypostsynapticpotentialenhancement:①thereducedinhibition②excitabilitysupernormal③highfrequencyexcitatorypotentials:themagnesiumionmediatedvoltagedependentonthetypeofreceptorinhibitionresultedindiminishedexcitatoryaminoacidreceptoractivityisincreasedthecauseofepilepticdischargesinthereleaseofotherneurotransmitters,atthesametime,thecentralsomeendogenousvoltagedependentcurrentcanalsobedirectlyincreasesinexcitatorypostsynapticdepolarizationofeffectiveness,includingslowinactivationofsodium,calciumcurrentandmayrepresentthecalciumdependentactionpotentialsandtransientcalciumcurrentThesemechanismstogethercontributedtoweakexcitatorysynapticcurrentstothegreatpainofthepostsynapticpotentialtransformation阵发性去极化漂移的产生主要与神经元内环境改变和突触功能的异常有关,但也与人的易感性有关。在没有外源性致痛因索作用下,很多机制对这种内源性暴发倾向有调节作用,而在病理条件下,由于神经递质异常,减少了钾离子电流细胞外钾离子浓度增加和钙离子减少改变了膜电位特征损伤后通道的再分布和解剖关系紊乱以及在慢性癫痫中所见到的失神经损伤都可能改变人的易感性,从另一方断促成巨大突触后电位的形成。Paroxysmaldepolarizingshiftresultingmainlyfromtheenvironmentalchangeinneuronsandsynapticfunctionabnormalities,butalsowiththepeoplerelatedtosusceptibilityIntheabsenceofexogenousinducedpainundertheactionofmanyfactors,mechanismofthisendogenousoutbreakstendtohavearegulatoryrole,andinpathologicalconditions,duetoneurotransmitterabnormalities,reducedthepotassiumcurrentextracellularpotassiumionconcentrationincreasedandcalciumwasreducedbychangingthemembranepotentialafterinjurycharacteristicschanneldistributionandtheanatomicrelationshipbetweenthedisturbanceaswellasinchronicepilepsyinseelossofnerveinjurymayalterthesusceptibility,fromanothersidethefaultcontributedtogreatpostsynapticpotentialformation虽然都有阵发性去极化漂移,但不同脑区出现不同类型癫痫的原因是:①不同神经元离子通道的位置和密度不同②内源性电流间及生理条件下突触电流的相互作用不同③不同脑区局部神经元的类型不同,异常激活和放电扩布经过的脑组织数量和部位不等④能通过第二信号系统改变电压依赖型膜电流的内源性突触调质的释放不同。癫痫起始神经元的癫痫放电尚需在局部兴奋环路中被强化。慢性的是由于损伤后轴突再生,急性的是由于与神经元高频活动有关的轴突传出增强所致,而这种与神经元高频放电有关的轴突传出增加与NMDA募集有关。谷氨酸、门冬氨酸受体或通道复合物在正常轴突传递中是相对静止的,当神经元处于静息电位时其受到周围镁离子的抑制,神经元除极时,镁离子抑制作用减弱,增加神经元的除极作用,随着大量兴奋性神经递质释放,更多的除极通道被激活。同时,由于神经元的除极化,一个或更多的电压门控钙通道开放,通过此通道产生的电流参与了神经元的除极活动,在兴奋性轴突和环路作用下形成正反馈,出现一系列反复的激活,促使神经元过度同步化。这种同步化的癫痫放电可在同类神经元中传播或通过轴突或突触传到其他类型的神经元,如从海马CA区到海马C区的锥体细胞也可从深层锥体细胞到同柱表层的锥体细胞或经皮质一皮质通路到远端锥体细胞。Althoughbothhaveaparoxysmaldepolarizingshift,butdifferentbrainregionsappearindifferenttypesofepilepsyiscausedby:①differentneuronalionchannellocationanddifferentdensity②endogenouscurrentandphysiologicalconditionsofsynapticcurrentsintheinteractionofdifferentthedifferentbrainregionsoflocalneuralelementtypes,abnormalactivationandspreadingafterdischargebraintissuevolumeandpartsofunequal④canpassthesecondsignalsystemtochangethevoltagedependentmembranecurrentsofendogenoussynapticreleaseofdifferentquenchingandtemperingEpilepticneuronsinepilepticdischargeisneededinthelocalexcitationloopisstrengthenedinChronicisduetoaxonalregenerationafterinjury,acuteisduetohighfrequencyandneuronalactivityrelatedtoefferentaxonsandneuronscausedbytheenhancement,andthehighfrequencydischargerelatedefferentaxonsincreasewithNMDArecruitmentrelatedGlutamate,aspartatereceptororchannelcomplexesinnormalaxonaltransmissionisrelativelystatic,whenneuronsintherestingpotentialisaroundthemagnesiumioninhibition,neuronaldepolarization,magnesiumioninhibitionattenuates,increasedneuronaldepolarizationeffect,alongwiththemassivereleaseofexcitatoryneurotransmitters,morethanmostchannelsareactivatedAtthesametime,duetoneuronaldepolarization,oneormoreofthevoltagegatedcalciumchannelsopen,throughthispassagetogeneratecurrentinneuronaldepolarization,inexcitatoryaxonsandloopformedundertheeffectofpositivefeedback,theemergenceofaseriesofrepeatedactivationofneurons,induceexcessivesynchronizationThissynchronizationofepilepticdischargescanbeinthesameneuronaxonorsynaptictransmissionorthroughtoothertypesofneurons,suchasfromtheCAregionofthehippocampustotheChippocampalpyramidalcellsAlsoavailablefromdeeppyramidalcellstothesamecolumnsurfaceofpyramidalcellsorbyacorticalpathwaytothefarendofthecorticalpyramidalcells当一组神经元被激活或抑制时产生的信号通过全脑,在不同的循环中,抑制电位将使这种被异常激活的冲动逐渐减弱或消失,增强电位则将这种似乎随机的活动逐步引向高度同步化的放电,并波及远处的神经元。脊椎动物皮质正常显微结构和生理功能有利于高度同步化的发展,当形成一种特殊模式时,就引起阵发性高度去极化漂移。在皮质出现癫痫放电时,在病灶中心及周围还可记录到一个大而长的超极化电位。实验证实这种HP是产生EEG上棘慢复合波中慢波的原因,其形成机制主要是突触抑制,尤其是与GABA。受体作用有关的突触抑制。由GABA介导的快、慢性突触抑制在皮质中广泛存在,并且是有力的,可以向前或向后反馈,例如,当锥体细胞放电时,激活抑制性中间神经元,从而反回去抑制神经元放电,所以抑制性突触放电可以切断癫痫放电和阻止其在皮质中的传播。另外,在阵发性去极化漂移中出现的大量钙依赖型电流也可限制兴奋持续的时间,有助于SIP的形成。正是由于这种紧接着去极化后出现的IMP电位的存在使癫痫放电被限制在局部而不出现临床发作。Whenagroupofneuronsareactivatedorinhibitedwhenthesignalisgeneratedbythebrain,ineachcycle,inhibitorypotentialoftheabnormalactivationoftheimpulsewasgraduallydiminishedordisappeared,enhancedpotentialistheseeminglyrandomeventstohighlysynchronizeddischarge,andspreadtodistantneuronsVertebratecortexofnormalmicrostructureandphysiologicalfunctionfacilitateshighlysynchronizeddevelopment,whentheformationofaspecialmode,iscausedbyparoxysmaldepolarizationshiftheightInthecorticalseizuredischarge,inthecenterofthelesionandthesurroundingcanalsoberecordedintoalargeandlonghyperpolarizingpotentialsTheexperimentprovesthiskindofHPisEEGspikeandslowwavecomplexofslowwavesinreason,mechanismofitsformationismainlysynapticinhibition,especiallywithGABAReceptoronsynapticinhibitionMediatedbyGABAfastsynapticinhibitioninthecortexofchronic,widespread,andispowerful,canbemovedforwardorbackwardfeedback,forexample,whenthepyramidalcelldischarge,activationofinhibitoryinterneurons,whichagaininhibitionneurons,sotheinhibitorysynapticdischargecancutofftheepilepticdischargeandtopreventitincortexPropagationInaddition,inparoxysmaldepolarizingshiftoccursinacalciumdependentcurrentmayalsobelimitingtheexcitotoxicduration,contributetotheformationofSIPItisbecauseofthisfollowedbydepolarizationoccursaftertheIMPpotentialsinepilepticdischargeswerelimitedtolocalwithoutclinicalseizures人利用部分性癫痫模型观察过癫痫放电产生的全过程:首先是病灶细胞外钾离子增加和钙离子减少,随后有成千上万神经元开始同步异常放电,形成一个称为阵发性去极化漂移的巨大电位,紧接着有一个过度去极化,出现病灶周围神经元的抑制。病灶神经元远端投射区的神经元可有短暂性兴奋,但大多数伴随着突触间的相互作用也被抑制,终止于病灶内的神经元可被逆点燃,产生动作电位逆行传播。由于病灶内紧随去极化后出现的超极化抑制使大多数发作间期的病样放电被严格的局限在局部而表现为EEG上的癫痫放电,不会引发临床上的癫痫发作。Useofpartialepilepsymodeltoobserveepilepticdischargeprocess:thefirstisthelesionincreasedextracellularKandCaisreduced,thentensofthousandsofneuronsbegintosynchronousabnormaldischarge,formingaiscalledaparoxysmaldepolarizingshiftandhugepotential,tightandthereisanexcessivedepolarization,appearanceoflesionsofperipheralneuronsinhibitionofFociofneuronsprojectingdistallyofneuronsmayhavebeenshortofsexualexcitement,butmostaccompaniedbysynapticinteractionsaresuppressed,terminatinginalesionwithintheneuronscanbeinversetoignite,thegenerationofactionpotentialsofretrogradedisseminationAsaresultofintralesionalfollowedbydepolarizationoccursafterhyperpolarizinginhibitiontomakethemostofinterictalepileptiformdischargesofthediseaseisstrictlyconfinedinalocalandperformancefortheEEGepilepticdischarges,doesnotcauseclinicallyepilepticseizures()间歇期癫痫放电向发作的转化:对于间歇期痛性活动转变成临床发作已进行了许多系统的研究。痛性活动向发作的转化中发生了一系列的变化,使通常具有自限性的癫痫放电在时间和解剖空间上得以扩布,其中最重要的是阵发性去极化漂移后过度去极化消失而被局部或远隔脑区的除极化替代,使病灶周围的抑制减弱。在癫痫放电形成的过程中,病灶内高度去极化后的HP形成后如不能完全抑制病灶周围或远处神经元的兴奋性活动,这种兴奋性活动将诱导抑制功能的减弱,此时,癫痫放电就有可能通过正常轴突通路和生理机制向邻近脑区传播,将放电传向下一个神经元,并进人其投射区,经兴奋性连接环路再返回放电区,反复多次重复循环,使以前似乎随机的放电经其循环通路中多个释站的增益和导向,逐渐形成集中的高频放电,这种高频放电可通过轴突前、后机制引起高频兴奋性突触后电位,同时,随着突触后神经元的去极化,有更多受体被激活,产生更多的去极化,使更多的钙流入细胞内,引起兴奋性轴突效益持续性增强,在一些其他机制的参与下进一步强化这条通路的作用。()intermittentperiodsofepilepticdischargestoattackTransformation:forintermittentpainfulactivitiesintoclinicalseizureshasbeencarriedoutinmanysystemsresearchThepainfulmotiontoattacktransformationhappenedaseriesofchange,sothatusuallyselflimitedepilepticdischargesintemporalandanatomicalspacetospread,ofwhichthemostimportantisaparoxysmaldepolarizingshiftafterexcessivedepolarizationdisappearedbylocalordistantbrainareasforgenerationofdepolarization,thelesionsaroundthereducedinhibitionIntheepilepticdischargesintheprocessoftheformation,intralesionalhighlydepolarizedafterHPformationafterifnotcompletelyinhibitedlesionoftheperipheralordistantneuronalexcitability,theexcitatoryactivityinducedinhibitionoffunctionabate,atthistime,epilepticdischargeispossiblethroughthenormalaxonpathwaysandphysiologicalmechanismtotheneighboringbrainregionsofcommunication,willbedischargedownaneuron,andtheprojectionarea,theexcitatoryconnectionloopreturndischargezone,repeatedseveraltimestorepeatthecycle,sothatthepreviouslyappearedtorandomdischargethroughthecirculationpathmultiplereleasestationgainandaguide,graduallyformedfocusedhighfrequencydischarge,thehighfrequencydischargethroughtheprecedingaxonafterthemechanism,causehighfrequencyofexcitatorypostsynapticpotentials,atthesametime,alongwiththepostsynapticneurondepolarization,withmorereceptorsareactivated,resultinginmoredepolarized,makemorecalciuminfluxintothecell,causingexcitatoryaxonbenefitscontinuetostrengthen,insomeothermechanismsinvolvedinfurtherstrengtheningthispatheffectof兴奋作用增加的同时,抑制作用可能进一步减弱。正常情况下CABA的抑制作用是很强的,但抑制性突触似乎对高频活动更敏感,所以兴奋性作用的增强减少了抑制性突触的效能,加速了痛性活动的产生和传播,兴奋增强和抑制减弱的双重作用使越来越多的区域进人发作中。向下一个神经元的传播使原发性放电区域的轴突末梢因神经递质的释放和细胞外钾离子的积蓄被激活,轴浆流逆行,脑激活区从局部上行通过侧支联系到许多其他区域。这样,发作活动就能从局部异常区传播到其他非癫痫区,扩布的范围和速度取决于病灶区的连接、原发性放电的强度和接收脑区的状态。“此时,至少在急性病灶区可以发现阵发性去极化漂移后过度去极化逐渐变小,并消失,而被初期类似小阵发性去极化漂移的去极化波代替,在几次成功的癫痫放电后,E}上就出现后放电,随着每一次间歇期放电,后放电越来越大,附近脑和远隔区域也逐渐加人到发作中来,使异常放电逐步扩布,最后进入临床发作”。这种癫痫放电向发作的转变可以由局部放电的“逃脱”或放电向脑附近或远处传播所引起。临床和实验都证实间歇期癫痫放电向发作的转化是由于多重机制的作用,兴奋及过度同步化增强、抑制作用减弱、非特异性诱导因素的共同作用促成了发作间期癫痫放电向发作的转变。Excitatoryeffectsofincreasedatthesametime,inhibitionmayweakenfurtherUndernormalcircumstances,theinhibitoryeffectofCABAisverystrong,butinhibitorysynapticactivityseemstobemoresensitivetohighfrequency,sotheexcitatoryroleenhancementreducesinhibitorysynapticefficacy,acceleratingthepainfulmotiongenerationandpropagation,excitabilityenhancementandinhibitionofweakeningthedualrolemakesmoreandmoreareaintotheattackDownaneuronalcommunicationmakesprimarydischargeregionsoftheaxonendingsforneurotransmitterreleaseandextracellularpotassiumsavingsisactivated,axoplasmicretrogradeflow,brainactivationregionfromthelocaluplinkviacollateralconnectionstomanyotherareasThus,seizureactivitycanfromtheanomalousareaspreadtoothernonepilepticzone,spreadingrangeandspeeddependingonthelesionareaconnection,primarydischargeintensityandreceptionareasofthebrainstate"Atthistime,atleastintheacutelesionareacanbefoundinparoxysmaldepolarizingshiftafterexcessivedepolarizationdecreasedgradually,anddisappeared,andwasinitiallysimilartosmallparoxysmaldepolarizingshiftofthedepolarizationwaveinstead,afterseveralsuccessfulepilepticdischarges,E}willappearafterdischarge,witheachperiodofintermittentdischarge,afterdischargeismoreandmorebig,nearbrainandremoteregionalsograduallyincreasetotheonsetofabnormaldischarge,sothatgraduallyspread,finallyenteringclinicalseizures"Thiskindofepilepticdischargestoattackthetransformationcanbecomposedofpartialdischarge"escape"ordischargetobraininnearordistantspreadcausedbyClinicalandexperimenthasconfirmedthatintermittentperiodsofepilepticdischargestoattacktransformationwasduetomultiplemechanismsofaction,excitementandexcessivesynchronization,enhancedinhibitionattenuates,nonspecificinduciblefactorscontributedtotheinterictalepilepticdischargestoattackchange通过以上的介绍,相信很多人对癫痫放电的产生都有了一定的认识和了解,虽然看起来有点繁琐,但这些介绍都是经过专家研究和实践所得出的结果,希望对大家能够有所帮助。本文转载自:

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