臨床神經(jīng)病學(xué)課件：20 顱內(nèi)高壓

IntracranialHypertensionIntracranialpressureIntracranialpressureistheresultofaconstantlychanginginterplaybetweentheCSFsystem,thecerebralbloodvolumecontainedinvenous,capillaryandarterialvesselsandbraintissuewithitsassociatedintra-andextracellularfluid.Eachofthesesystemsexertsaninfluenceandtheend-result,atequilibrium,iscalledICP.NormalICPAgegroupNormalrange(mmHg)Adultsandolderchildren

10-15

Youngchildren3-7Terminfant1.5-6Braintissue：85%neuron500-700mlglialcell700-900ml

extracellularfluid100-150mlCSF10%100-150mlCBF2-7%70-100mlBLOODExtracellularfluidCSFNeuronGlialcellIntracranialpressureMonro-kelliehypothesisThesumoftheintracranialvolumesofblood,brain,CSF,andothercomponentisconstant,andthatanincreaseinanyoneofthesemustbeoffsetbyanequaldecreaseinanother,orelsepressurewillrise.Thepressure-volumecurveICPautoregulation1CSFandICP

CSFtotal150mlvolumeformationrate0.3-0.35ml/min

ICP↑→

CSFisproduced↓→CSFvolume↓→ICP↓

ICP↑→

CSFisabsorbed→CSFvolume↓→ICP↓

2braintissueandICP3cerebralbloodflow(CBF)andICP

CPP=MAP-JVP=MAP—ICP

CPPCVRMAP-ICPCVRCBF=EffectsofvariationsinCBF

CBF(mlper100gmtissue/min)Condition45-65Normalbrainatrest75-80graymatter20-30whitematter25EEGbecomesflatline15Physiologicparalysis12Brainstemauditoryevokedresponsechanges10Alterationsincellmembranetransport(celldeath)CausesofraisedintracranialpressureMasslesionsintracranialhaematoma,cerebralcontusion,tumor,abscessVascularfactorspassivearterialdilatationbylossofautoregulationandraisedarterialbloodpressurevenouscongestionbysinusocclusionNon-vascularfactors

hydrocephalus,edemaMasslesionstumorhematomaVascularfactorsCPP：180mmHg----50mmHg.Contussion,lacerationgandedemahydrocephalusPresentationofIC-HTNHeadaches

Classicallydescribedasbeingworseinthemorning(possiblyduetohypoventillationduringsleep)

Oftenexacerbatedbycoughing,straining,orbendingforward.

PresentationofIC-HTNVomitingPapilledemaPresentationofIC-HTN

Cushing’striad1hypertension2bradycardia3respiratoryirregularityIC-HTNtreatmentmeasuresGoals:keepICP<20mmHgCPP>60mmHgIC-HTNtreatmentmeasuresIC-HTNtreatmentmeasures“Secondtier”therapyforpersistentIC-HTNHighdosebarbitureatetherapy:initiateifICPremains>20-25mmHgHyperventilatetopCO2=25-30mmHg.HypothermiaDecompressivecraniectomy:removalofportionofcalvariaand/orlargeareasofcontusedhemorrhagicbrain(makesroomimmediately;removesregionofdisruptedBBB).Controversial(mayenhancecerebraledemaformation).Ifcontused,considertemporaltiplobectomy(nomorethan4-5cmondominantside,6-7cmonnon-dominant)(totaltemporallobectomyisprobablytooaggressive)orfrontallobectomy.HasnotshowngreattherapeuticpromiseHypertensivetherapyBrainHerniationShiftsinbraintissuethroughrigidopeningsintheskullcompressotherstructuresoftheCNSproducingtheobservedsymptoms.一、小腦幕裂孔疝

（Transtentorialherniation）最常見的一種腦疝。顳葉的鉤回、海馬回和臨近的舌回受顳葉或大腦半球占位的壓迫，向內(nèi)下移位疝入小腦幕裂孔，壓迫中腦、動眼神經(jīng)和后交通動脈等。

臨床表現(xiàn)動眼神經(jīng)麻痹—病理性瞳孔散大，光反射消失，眼球外展，眼瞼下垂。中腦受壓—意識障礙，對側(cè)肢體癱瘓，自主運動少，肌張力增高，肌力減退腱反射亢進，錐體束征陽性。進一步加重，昏迷加深，動眼神經(jīng)核進一步受到損害，出現(xiàn)雙側(cè)瞳孔散大，雙側(cè)肢體癱瘓，去大腦強直。亦稱小腦扁桃體疝

后顱凹占位或幕上

占位引起的嚴(yán)重顱

內(nèi)壓高，導(dǎo)致小腦

扁桃體下移進入枕

大孔和錐管，使延

髓受壓，延髓軸向

和偏向移位，神經(jīng)

受到牽張。二、枕大孔疝

（Foramenmegnumherniation）臨床表現(xiàn)頸神經(jīng)根牽張頸后部疼痛，頸項強直，強迫頭位四腦室激惹反復(fù)吐后顱神經(jīng)核功能紊亂，吞咽困難,呼吸、脈搏減慢，血壓升高,強迫頭位。進一步加重，腦脊液循環(huán)障礙。扁桃體充血、水腫、壞死以及咳嗽等用力動