Objective:TodiscussthemechanismofcerebralvesselspasmcausedbyconcussionandtheeffectofNimodipineonconcussion.Methods:Atotalof224patientswhoweretreatedfromMarch1995toOctober1999werepidedintotwogroupsrandomly,ie.Nimodipinegroup(113cases)andcontrolgroup(11cases).Middlecerebralartery(MCA),basilarartery(BA)andtheaveragepeakforwardvelocityofcerebralbloodflowwereobservedbycolorthree-dimensionaltranscranialDoppler(3D-TCD)within24hoursafteradmissionandattheendof3-6daysoftreatment.Cerbralbloodflowchanges,characteristicsandtreatmenteffectwereanalyzedanddeterminedbyclinicalmainsymptomdisappearancerate.Results:Inconcussion,cerebralbloodflowwaspidedinto3phases:cerebralbloodflowlowinfusiondilationphase,cerebralbloodvesselspasmphaseandcerebralbloodflowrecoveryphase.IntheNimodipinegroup,clinicalmainsymptomdisappearanceratewashigherthanthatinthecontrolgroupinthecerebralspasmandrecoveryphaseswithasignificantdifference(P<0.01).Conclusions:Cerebralvesselspasm,hypoxiaandischemialesionarethemainpathologicalchanges.Whethercerebraldysfunctionisreversibleornotismainlydeterminedbyspasmtimeofcerebralbloodvessel.Nimodipinehasagoodeffectonreleasingspasmanddiminishingthecerebralbloodfolwvelicity.Itnotonlyimprovescurativeeffectonconcussion,butalsoreducesandpreventsconcussionsequelae.Hence,concussionpatientswhohavecerebralspasmconfirmedby3D-TCDshouldbegivenNimodipineroutinelyandearly.
