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TUBERCULOUSMENINGITIS结核性脑膜炎LongnanHospitalChenjingTUBERCULOUSMENINGITIS结核性脑膜炎Lo1Tuberculousmeningitisisaninfectionofthemembranes

膜coveringthebrainandspinalcord(meninges).Tuberculosis(TB)iscausedbythebacteriumMycobacteriumtuberculosis结核分枝杆菌andisannuallyresponsiblefornearlytwomilliondeathsworldwide.Athirdoftheworld'spopulationiscurrentlyinfectedwiththeTBbacillus,andmorethaneightmillionnewcasesarediagnosedeachyear.TuberculousmeningitisisaniTuberculousmeningitismustbeconsideredinpatientswhopresentwithaconfusionalstate,especiallyifthereisahistoryofpulmonarytuberculosis,alcoholism,corticosteroidtreatment,HIVinfection,orotherconditionassociatedwithimpairedimmuneresponses.TuberculousmeningitismustbeItshouldalsobeconsideredinpatientsformareas(eg,Asia,Africa)orgroups(eg,thehomelessandinner-citydrugusers)withahighincidenceoftuberculosis.ItshouldalsobeconsiderediCausesRiskfactorsincludeahistoryof:

AIDSExcessivealcoholusePulmonarytuberculosisWeakenedimmunesystemCauses中枢神经系统感染ppt课件中枢神经系统感染ppt课件中枢神经系统感染ppt课件Pathogenesis&Pathology发病机制&病理Tuberculousmeningitisusuallyresultsfromreactivationoflatentinfectionwithmycobacteriumtuberculosis.结核性脑膜炎多是由于潜伏的结核杆菌复发感染引起的。Pathogenesis&Pathology发病机制&病Primaryinfection,typicallyacquiredbyinhalingbacilluscontainingdroplets,maybeassociatedwithmetastaticdisseminationofblood-bornebacillifromthelungstothemeningesandsurfaceofthebrain.

Heretheorganismsremaininadormantstateintuberclesthatcanruptureintothesubarachnoidspaceatalatertime,resultingintuberculousmeningitis.

原发性感染,尤其是通过吸入含菌颗粒引起的感染,可能与血源性细菌从肺部到脑膜及大脑表面的播散有关。此处的致病菌在结核结节中处于休眠状态,后期可破入蛛网膜下腔,并导致结核菌性脑膜炎。Primaryinfection,typicallya主要发现是含有大量单核细胞的脑基底部脑膜分泌物。脑膜及脑表面可见结核结节。Themainfindingisabasalmeningealexudate渗出物containingprimarilymononuclearcells.Tuberclesmaybeseenonthemeningesandsurfacesofthebrain.主要发现是含有大量单核细胞的脑基底部脑膜分泌物。脑膜及脑表面Theventriclemaybeenlargedasaresultofhydrocephalus,andtheirsurfacesmayshowependymalexudateorgranularependymitis.

Arteritiscanresultincerebralinfarction,andbasalinflammationandfibrosiscancompresscranialnerves.

脑积水可引起脑室扩大,并且脑室表面可有大量室管膜渗出物或颗粒状室管膜炎。动脉炎可导致脑梗塞,而颅底部炎症反应和纤维化可压迫神经。TheventriclemaybeenlargedAcutetuberculousmeningitiswithmarkedinvolvementofthevesselwallsandocclusionofsmallervessels.Thevascularinvolvementcanresultininfarction.Acutetuberculousmeningitisw中枢神经系统感染ppt课件中枢神经系统感染ppt课件ClinicalFindings

A.SYMPTOMSSymptomshaveusuallybeenpresentforlessthan4weeksatthetimeofpresentationandincludefever,lethargy昏睡

orconfusion,andheadache.Weightloss,vomiting,neckstiffness,visualimpairment,diplopia复视,focalweakness,andseizuresmayalsooccur.Ahistoryofcontactwithknowncasesoftuberculosisisusuallyabsent.ClinicalFindingsA.SYMPTOMSB.SIGNSFever,signsofmeningealirritation脑膜刺激征,andaconfusionalstatearethemostcommonfindingsonphysicalexamination,butallmaybeabsent.Papilledema视乳头水肿,ocularpalsies眼肌麻痹,andhemiparesis轻偏瘫

aresometimesseen.B.SIGNSFever,signsofmeningeComplicationsincludespinalsubarachnoidblock脊髓蛛网膜下腔梗阻,hydrocephalus脑积水,brainedema脑水肿,cranialneverpalsies颅神经麻痹,andstrokecausedbyvasculitisorcompressionofbloodvesselsatthebaseofthebrain因血管炎或颅底血管受压导致的卒中.Complicationsincludespinals结核球结核球strokestrokehydrocephalushydrocephalusLaboratoryFindings

Onlyone-halftotwo-thirdofpatientsshowapositiveskintestfortuberculosisorevidenceofactiveorhealedtubercularinfectiononchestx-ray.LaboratoryFindingsOnlyone-hCSFThediagnosisisestablishedbyCSFanalysis.CSFpressureisusuallyincreased,andthefluidistypicallyclearandcolorlessbutmayformaclotuponstanding.Lymphocyticandmononuclearcellpleocytosisof50-500cells/mLismostoftenseen,butpolymorphonuclear多形核细胞pleocytosiscanoccurearlyandmaygiveanerroneousimpressionofbacterialmeningitis.CSFproteinisusuallymorethan100mg/dL,particularlyinpatientswithspinalsubarachnoidblock.Theglucoselevelisusuallydecreasedandmaybelessthan20mg/dL.CSFThediagnosisisestablisheAcid-fastsmears抗酸染色涂片ofCSFshouldbeperformedinallcasesofsuspectedtuberculousmeningitis,buttheyarepositiveinonlyaminorityofcases.Acid-fastsmears抗酸染色涂片ofCSFDefinitivediagnosisismostoftenmadebyculturingMtuberculosisfromtheCSF,aprocessthatusuallytakesseveralweeksandrequireslargequantitiesofspinalfluidformaximumyield.Definitivediagnosisismosto中枢神经系统感染ppt课件中枢神经系统感染ppt课件Thepolymerasechainreaction(PCR)聚合酶链反应

hasalsobeenusedfordiagnosis.ThepolymerasechainreactionFinally,theCTscanmayshowcontrastenhancementofthebasalcisternsandcorticalmeninges,orhydrocephalus.Finally,theCTscanmayshowMRIappearanceofthetypicalpatternofcentralnervoussystemtuberculousmeningitisMRIappearanceofthetypicalDifferentialDiagnosisManyotherconditionscanasubacuteconfusionalstatewithmononuclearcell单核细胞pleocytosis脑脊液细胞增多,includingsyphilitic梅毒的,fungal,neoplastic肿瘤的,andpartiallytreatedbacterialmeningitis.Thesecanbediagnosedbyappropriatesmears涂片,cultures,andserologic血清学的andcytologicexaminations细胞学检查.DifferentialDiagnosisManyothTreatmentTreatmentshouldbestartedasearlyaspossible;itshouldnotbewithheldwhileawaitingcultureresults.ThedecisiontotreatisbasedontheCSFfindingsdescribedabove;lymphocyticpleocytosisanddecreasedglucoseareparticularlysuggestive,evenifacid-fastsmearsarenegative.综合治疗:药物治疗、全身支持、并发症的预防、耐药与多耐药TB菌感染的治疗、对症治疗。药物治疗原则:早期、联合、足量、长期、顿服TreatmentTreatmentshouldbesDRUGSFourdrugsareusedforinitialtherapy,untilcultureandsusceptibilitytestresultsareknown.四联治疗isoniazid,异烟肼300mg;rifampin,利福平600mg;pyrazinamide,吡嗪酰胺25mg/kg;ethambutol,乙胺丁醇15mg/kg,eachgivenorallyoncedaily.DRUGSFourdrugsareusedforiForsusceptiblestrains,ethambutol乙胺丁醇canbediscontinued,andtripletherapycontinuedfor2months,followedby4-10monthsoftreatmentwithisoniazid异烟肼andrifampin利福平alone.Pyridoxine,维生素B650mg/d,canbeusedtodecreasethelikelihood可能性ofisoniazid-inducedpolyneuropathy.Forsusceptiblestrains,ethamSideeffectofdrugsComplicationsoftherapyinclude:hepatic肝脏的dysfunction(isoniazid异烟肼,rifampin利福平,andpyrazinamide吡嗪酰胺

)polyneuropathy多神经炎

(isoniazid)opticneuritis(ethambutol乙胺丁醇)seizures(isoniazid)ototoxicity耳毒性(streptomycin链霉素)SideeffectofdrugsComplicatiCorticosteroidsPrednisone泼尼松60mg/dorallyinadultsor1-3mg/kg/dorallyinchildren,taperedgraduallyover3-4weeksCorticosteroidsareindicatedasadjunctive辅助的therapyinpatientswithspinalsubarachnoidblock.Theymayalsobeindicatedinseriouslyillpatientswithfocalneurologicsignsorwithincreasedintracranialpressurefromcerebraledema.CorticosteroidsPrednisone泼尼松Theriskofusingcorticosteroidsmaybehigh,howeverespeciallyiftuberculousmeningitishasbeenmistakenlydiagnosedinapatientwithfungalmeningitis.Therefore,iffungalmeningitishasnotbeenexcluded,antifungaltherapyshouldbeaddedalongwithcorticosteroids.TheriskofusingcorticosteroPrognosisEvenwithappropriatetreatment,aboutone-thirdofpatientswithtuberculousmeningitissuccumb死.Comaatthetimeofpresentationisthemostsignificantpredictorofapoorprognosis.PrognosisEvenwithappropriateCerebralCysticercosis脑囊虫病CerebralCysticercosis脑囊虫病CysticercosisiscommoninMexico,CentralandSouthAmerica,westernandsouthernAfrica,India,China,andsoutheastAsia.CysticercosisiscommoninMexThediseasefollowsingestionoflarvae幼虫

oftheporktapeworm(taeniasolium-猪肉绦虫)andaffectsthebrainin60-90%ofcases.Thediseasefollowsingestion中枢神经系统感染ppt课件Pathology病理上典型的包囊大小为5~10mm,可有薄壁,或呈多个囊腔,内有囊尾蚴。囊虫的囊尾蚴囊肿常为圆形或卵圆形,内膜上有一小白色的囊虫结节突起。当虫体死亡或液化时,囊腔内为暗褐色混浊液体,内含大量蛋白质、当虫体液化被吸收后囊腔变小,囊壁增厚,囊虫死后常发生钙化。

Pathology病理上典型的包囊大小为5~10mm,可有薄中枢神经系统感染ppt课件中枢神经系统感染ppt课件中枢神经系统感染ppt课件中枢神经系统感染ppt课件中枢神经系统感染ppt课件ClinicalFindingLarvaeundergohematogenous血源性dissemination,formingcysts囊肿

inthebrain,ventricles脑室,andsubarachnoidspace.Neurologicmanifestationsofcysticercosisresultfrom1.themasseffect占位效应

ofintraparenchymal脑实质内cysts2.obstructionofCSFflowbyintraventricularcysts3.inflammationthatcausebasilarmeningitis.ClinicalFindingLarvaeundergoTheyincludeseizures,headache,focalneurologicsigns,hydrocephalus脑积水,myelopathy脊髓病,andsubacutemeningitis.Peripheralbloodeosinophilia嗜酸性细胞增多症,softtissuecalcifications钙化,orparasites寄生虫

inthestool粪便suggestthediagnosis.Theyincludeseizures,headach

LaboratoryFindings

TheCSFtypicallyshowsalymphocyticpleocytosis(<100cells/mL),witheosinophils嗜酸细胞usuallypresent.Openingpressureisoftenincreasedbutmaybedecreasedwithspinalsubarachnoidblock;ifthisissuspectedmyelography椎管造影术shouldbeperformed.Proteinisincreasedto50-100mg/dL,andglucoseis20-50mg/dLinmostcases.Complementfixation补体结合andhemagglutination红血球凝聚studiescanassistinthediagnosis.LaboratoryFindingsTheCSFtTheCTscanorMRImayshowcontrast-enhancedmasslesionswithsurroundingedema,intracerebralcalcifications,orventricularenlargement.

TheCTscanorMRImayshowcoMRI活动期:T1加权像囊虫呈圆形低信号,头节呈点状或逗点状高信号,T2加权像囊虫呈圆形高信号,头节呈点状低信号。退变死亡期:T1加权像水肿区低信号内有高信号环或结节,或仅有低信号区;T2加权像水肿区高信号,内有低信号环或结节。非活动期:T1\T2加权像上多呈圆形低信号。混杂期:T1\T2加权像上均呈混杂密度病灶。MRI活动期:T1加权像囊虫呈圆形低信号,头节呈点Vesicular囊状的colloidal胶体的granular颗粒状的calcified钙化的Vesicular囊状的col中枢神经系统感染ppt课件中枢神经系统感染ppt课件中枢神经系统感染ppt课件

AxialbrainMRI.aT1-W,bT2-W,cFLAIRanddcontrast-enhancedT1-Wsequences.Imagesrevealinnumerablecystsinbilateralbasalganglia(arrowsinaandb)andcerebralhemispheres,givingthe“starry-sky”pattern.Afewlesionsdemonstrateperifocaloedemaandring-enhancement(arrowsincandd)suggestiveofthecolloidvesicularstageAxialbrainMRI.aT1-W,MRI.SagittalbrainT2-Wimagesshowcysticerciintheextra-orbitalmuscles(arrow)(a)andtongue(arrows)(b)aswellasinthecranialandcervicalmuscles.cSagittalspineT2-Wimagerevealshyperintenselesionsinnearlyeveryparaspinalmuscle(arrows)MRI.SagittalbrainT2-WimageTreatmentTheindicationsoftreatmentofcerebralcysticercosisarecontro

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