急性一氧化碳中毒脑损伤及延迟神经后遗症的神经保护治疗：捆绑疗法一氧化碳中毒是全球最常见的中毒死亡原因之一。在韩国，由一氧化碳中毒引起的死亡人数迅速增加，这与越来越多的人燃烧木炭自杀未遂有关。40％的幸存者在2-40天内会发展为延迟神经后遗症，在急性期会出现包括头痛、头晕//晕厥、意识丧失//惊厥、昏迷和死亡。在延迟期，患者会出现包括记忆丧失、运动障碍、帕金森症类似的综合征、沟通障碍、抑郁的情绪、痴呆和精神错乱等症状。高压氧治疗在很大程度上取决于缺氧负荷，这也是目前其疗效存在争论的原因。韩国亚洲大学医学院的科学家和医生联合研究了一氧化碳中毒和延迟神经后遗症最新的发病机制。潜在的机制包括缺氧负荷、氧化应激、脂质过氧化和儿茶酚胺的问题。儿茶酚胺是除多因素促发的病理生理学之外的一种新方法，从而推断急性一氧化碳重度患者双边基底神经节和苍白球的损伤与可卡因、海洛因//甲基苯丙胺的吸食者表现出相似的特性。基于病理生理学假定，包括高压氧、靶向温度管理//抗交感神经药、抗氧化剂和类固醇等治疗，被建议称为“捆绑疗法”，并有望成为有效的治疗急性一氧化碳中毒脑损伤及延迟神经后遗症的方法。然而，建议所推荐的病理生理学和治疗，个体与联合，有待进一步的调查来验证。总的说来，这一领域提高的科学和临床知识将帮助预防延迟神经后遗症，减轻一氧化碳中毒的症状。相关文章发表在《神经再生研究（英文版）》杂志2015年1月1期上。Article:"Acutecarbonmonoxidepoisoninganddelayedneurologicalsequelae:apotentialneuroprotectionbundletherapy"bySunghoOh,Sang-CheonChoi(DepartmentofEmergencyMedicine,AjouUniversitySchoolofMedicine,Suwon,RepublicofKorea)OhS,ChoiSC(2015)Acutecarbonmonoxidepoisoninganddelayedneurologicalsequelae:apotentialneuroprotectionbundletherapy.NeuralRegenRes10(1):36-38.欲获更多资讯：NeuralRegenResTitleAPotentialBundleTherapyforNeuroprotectioninAcuteCarbonMonoxidePoisoningSummarystatementTheoptimaltherapiesforacutecarbonmonoxide(CO)poisoninganddelayedneurologicalsequelae(DNS)arecurrentlyunknown.Hyperbaricoxygentherapyiswell-known,butitsuseiscontroversialduetolackofevidencesregardingitsefficacy.Aseriesoftreatmentsasabundletherapy,withtargetedtemperaturemanagementasthebasetreatmentmayholdagreatpotentialafterscientificandclinicalvalidationstudies.BodyCOpoisoningisoneofthemostcommonpoisoningdeathsintheworld.InSouthKorea,thenumberofcarbonmonoxidepoisoningdeathshasrapidlyincreasedrecently,associatedwiththeincreasingnumberofsuicidalattemptsbyignitecharcoalburning.Upto40%ofthesurvivorsmaydevelopDNSin2to40days.Signsandsymptomsincludeheadaches,dizziness,syncope,lossofconsciousness,seizure,coma,anddeathduringtheacutephase.Duringthedelayedphase,theyincludememoryloss,movementdisorders,Parkinson-likesyndrome,communicationdisturbances,depressedmood,dementia,andpsychosis.Hyperbaricoxygentherapylargelydependsontheassumptionofhypoxicstress,hencethecurrentcontroversyoveritsefficacy.TheperspectivearticleispublishedinNeuralRegenerationResearch(Vol.x,No.xx,2015).ScientistsandphysiciansattheAjouUniversitySchoolofMedicinecollaboratedinresearchingforup-to-datepathophysiologicalmechanismsofacuteCOpoisoningandDNS.Theunderlyingmechanismswerehypoxicstress,oxidativestress,lipidperoxidation,andcatecholaminecrisis.Catecholaminecrisisisanoveladditiontothemulti-factorialpathophysiology,whichwasinferredfromthefactthatacuteCOpoisoningpatientssharesimilarcharacteristicsofthelesionsinthebilateralbasalgangliaandglobuspalliduswithsomeconsumersofcocaine,heroin,andmethamphetamine.Basedonthetentativepathophysiology,aseriesofpotentialeffectivetreatmentmethodsincludinghyperbaricoxygen,targetedtemperaturemanagement,sympatholytics,anti-oxidants,andsteroidsweresuggestedtobeusedasabundletherapy.Furtherinvestigationisnecessaryforvalidatingthesuggestedpathophysiologyandthetreatments,individuallyandcombined.Overall,improvedscientificandclinicalknowledgeinthisareawillhelppreventingDNSandminimizingthesignsandthesymptomsinCOpoisoning.Article:"Acutecarbonmonoxidepoisoninganddelayedneurologicalsequelae:apotentialneuroprotectionbundletherapy"bySunghoOh,Sang-CheonChoi(DepartmentofEmergencyMedicine,AjouUniversitySchoolofMedicine,Suwon,RepublicofKorea)OhS,ChoiSC(2015)Acutecarbonmonoxidepoisoninganddelayedneurologicalsequelae:apotentialneuroprotectionbundletherapy.NeuralRegenRes10(1):36-38.
