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1、P1:KVKmebr2004.cls(04/22/2004v1.1LaTeX2eMEBRdocumentclass)pp1311-mebr-492105September17,20043:6MetabolicBrainDisease,Vol.19,Nos.3/4,December2004(C2004)HypoglycemicBrainDamageRolandN.Auer1ReceivedNovember26,2003;acceptedDecember4,2004Hypoglycemiawaslongconsideredtokillneuronsbydeprivi
2、ngthemofglucose.Wenowknowthathypoglycemiakillsneuronsactivelyratherthanbystarvationfromwithin.Hy-poglycemiaonlycausesneuronaldeathwhentheEEGbecomesflat.Thisusuallyoccursafterglucoselevelshavefallenbelow1mM(18mg/dL)forsomeperiod.Atthattimeabruptenergyfailureoccurs,theexcitatoryaminoacid
3、aspartateismassivelyreleasedintothelimitedbrainextracellularspaceandfloodstheexcitatoryaminoacidreceptorslocatedonneuronaldendrites.Calciumfluxesoccurandmembranebreaksinthecellleadrapidlytoneuronalnecrosis.Significantneuronalnecrosisoccursafter30minofelectrocerebralsilence.Otherneurochem
4、icalchangesincludeenergydepletiontoroughly25%ofcontrol,phospholipaseandotherenzymeactivation,tissuealkalosis,andatendencyforallcellularredoxsystemstoshifttowardsoxidation.Hypoglycemiaoftendiffersfromischemiainitsneuropathologicdistribution,inthatnecrosisofthedentategyrusofthehippocamp
5、uscanoccurandapredilectionforthesuperficiallayersofthecortexissometimesseen.Cerebel-lumandbrainstemareuniversallysparedinhypoglycaemicbraindamage.Hypoglycemiaconstitutesauniquemetabolicbraininsult.Keywords:Hypoglycemia;metabolism;brain;necrosis;excitatoryaminoacids.HISTORICALASPECTSOFH
6、YPOGLYCEMIAManfredSakelintroducedhypoglycemiaasatherapyinpsychiatry(Sakel,1933,1934),publishedintheEnglishliteratureinthelate1930s(Sakel,1937).Atthattime,insulinwasgiventopeoplefortreatmentofschizophreniaanddrugaddiction.Thedesiredperiodofcoma,aftersomeexperiencewiththisprocedure,was3
7、0min,sinceitwasdiscoveredifthepatientremainedincomaforlongerthan30mincomawouldbetransformedfroma“reversiblecoma”toan“irreversiblecoma”(Baker,1938;Fazekasetal.,1951).Ourpresentdayunderstandingofhypoglycaemicbraindamagenowindicatesthatthiswasduetotherelativelyscantneuronalnecrosisthatoc
8、cursw