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TUBERCULOUSMENINGITIS结核性脑膜炎LongnanHospitalChenjingTuberculousmeningitisisaninfectionofthemembranes
膜coveringthebrainandspinalcord(meninges).Tuberculosis(TB)iscausedbythebacteriumMycobacteriumtuberculosis结核分枝杆菌andisannuallyresponsiblefornearlytwomilliondeathsworldwide.Athirdoftheworld'spopulationiscurrentlyinfectedwiththeTBbacillus,andmorethaneightmillionnewcasesarediagnosedeachyear.Tuberculousmeningitismustbeconsideredinpatientswhopresentwithaconfusionalstate,especiallyifthereisahistoryofpulmonarytuberculosis,alcoholism,corticosteroidtreatment,HIVinfection,orotherconditionassociatedwithimpairedimmuneresponses.Itshouldalsobeconsideredinpatientsformareas(eg,Asia,Africa)orgroups(eg,thehomelessandinner-citydrugusers)withahighincidenceoftuberculosis.CausesRiskfactorsincludeahistoryof:
AIDSExcessivealcoholusePulmonarytuberculosisWeakenedimmunesystemPathogenesis&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。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。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。Themainfindingisabasalmeningeal
exudate渗出物containingprimarilymononuclearcells.Tuberclesmaybeseenonthemeningesandsurfacesofthebrain.Theventriclemaybeenlargedasaresultofhydrocephalus,andtheirsurfacesmayshowependymal
exudateorgranularependymitis.
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。Acutetuberculousmeningitiswithmarkedinvolvementofthevesselwallsandocclusionofsmallervessels.Thevascularinvolvementcanresultininfarction.ClinicalFindings
A.SYMPTOMSSymptomshaveusuallybeenpresentforlessthan4weeksatthetimeofpresentationandincludefever,lethargy昏睡
orconfusion,andheadache.Weightloss,vomiting,neckstiffness,visualimpairment,diplopia
复视,focalweakness,andseizuresmayalsooccur.Ahistoryofcontactwithknowncasesoftuberculosisisusuallyabsent.B.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.Complicationsincludespinalsubarachnoidblock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.结核球strokehydrocephalusLaboratoryFindings
Onlyone-halftotwo-thirdofpatientsshowapositiveskintestfortuberculosisorevidenceofactiveorhealedtubercularinfectiononchestx-ray.CSFThediagnosisisestablishedbyCSFanalysis.CSFpressureisusuallyincreased,andthefluidistypicallyclearandcolorlessbutmayformaclotuponstanding.Lymphocyticandmononuclearcellpleocytosisof50-500cells/mLismostoftenseen,butpolymorphonuclear
多形核细胞pleocytosiscanoccurearlyandmaygiveanerroneousimpressionofbacterialmeningitis.CSFproteinisusuallymorethan100mg/dL,particularlyinpatientswithspinalsubarachnoidblock.Theglucoselevelisusuallydecreasedandmaybelessthan20mg/dL.Acid-fastsmears抗酸染色涂片ofCSFshouldbeperformedinallcasesofsuspectedtuberculousmeningitis,buttheyarepositiveinonlyaminorityofcases.DefinitivediagnosisismostoftenmadebyculturingMtuberculosisfromtheCSF,aprocessthatusuallytakesseveralweeksandrequireslargequantitiesofspinalfluidformaximumyield.Thepolymerasechainreaction(PCR)聚合酶链反应
hasalsobeenusedfordiagnosis.Finally,theCTscanmayshowcontrastenhancementofthebasalcisternsandcorticalmeninges,orhydrocephalus.MRIappearanceofthetypicalpatternofcentralnervoussystemtuberculousmeningitisDifferentialDiagnosisManyotherconditionscanasubacute
confusionalstatewithmononuclearcell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.TreatmentTreatmentshouldbestartedasearlyaspossible;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DRUGSFourdrugsareusedforinitialtherapy,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.Forsusceptiblestrains,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.SideeffectofdrugsComplicationsoftherapyinclude: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)CorticosteroidsPrednisone泼尼松60mg/dorallyinadultsor1-3mg/kg/dorallyinchildren,taperedgraduallyover3-4weeksCorticosteroidsareindicatedasadjunctive辅助的therapyinpatientswithspinalsubarachnoidblock.Theymayalsobeindicatedinseriouslyillpatientswithfocalneurologicsignsorwithincreasedintracranialpressurefromcerebraledema.Theriskofusingcorticosteroidsmaybehigh,howeverespeciallyiftuberculousmeningitishasbeenmistakenlydiagnosedinapatientwithfungalmeningitis.Therefore,iffungalmeningitishasnotbeenexcluded,antifungaltherapyshouldbeaddedalongwithcorticosteroids.PrognosisEvenwithappropriatetreatment,aboutone-thirdofpatientswithtuberculousmeningitissuccumb死.Comaatthetimeofpresentationisthemostsignificantpredictorofapoorprognosis.CerebralCysticercosis脑囊虫病CysticercosisiscommoninMexico,CentralandSouthAmerica,westernandsouthernAfrica,India,China,andsoutheastAsia.Thediseasefollowsingestionoflarvae幼虫
oftheporktapeworm(taenia
solium-猪肉绦虫)andaffectsthebrainin60-90%ofcases.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。
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.Theyincludeseizures,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.
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.TheCTscanorMRImayshowcontrast-enhancedmasslesionswithsurroundingedema,intracerebralcalcifications,orventricularenlargement.
MRI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。Vesicular囊状的colloidal胶体的granular颗粒状的calcified钙化的
AxialbrainMRI.aT1-W,bT2-W,cFLAIRanddcontrast-enhancedT1-Wsequences.Imagesrevealinnumerablecystsinbilateralbasalganglia(arrowsinaandb)andcerebralhemispheres,givingthe“starry-sky”pattern.Afewlesionsdemonstrateperifocal
oedemaandring-enhancement(arrowsincandd)suggestiveofthecolloidvesicularstageMRI.SagittalbrainT2-Wimagesshowcysticerciintheextra-orbitalmuscles(arrow)(a)andtongue(arrows)(b)aswellasinthecranialandcervicalmuscles.cSagittalspineT2-Wimagerevealshyperintenselesionsinnearlyeveryparaspinalmuscle(arrows)TreatmentTheindicationsoftreatmentofcerebralcysticercosisarecontrov
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