低血糖颅脑损伤.ppt

低血糖症相关的神经系统损害,HypoglycemiaindiabetesCryerPEetal.DiabetesCare.2003June;26（6）:1902-1912.,一次严重的医源性低血糖或由此诱发的心血管事件可能会抵消一生维持血糖在正常范围所带来的益处,高血糖,低血糖,高,低,低血糖诊断标准,对具体患者来说，个体的低血糖标准可能有较大差异，症状与血糖值可以不同步当血糖小于2.8mmol/L，可诊断为低血糖症一般患者发生低血糖时出现低血糖（Whipple）三联征，即：低血糖症状和体征；血糖浓度低；血糖浓度升高至正常水平时症状消失或显著减轻,引起低血糖的原因,最常见的是降糖药物使用不当所致。对胰岛素过度敏感。胰岛素过多：胰岛素瘤，异位胰岛素分泌瘤。反应性低血糖症：早期糖尿病，功能性低血糖，营养性低血糖肝脏疾病中毒：药物中毒，酒精中毒，大量食荔枝糖原累积病胃大部分切除术后肾上腺皮质或垂体前叶疾病,急性低血糖时的生理反应,增加拮抗激素的分泌，以拮抗胰岛素的作用，升高血糖使心血管系统发生相应变化，以利于葡萄糖在体内各种组织间的转运产生一系列预警症状，如饥饿，以迅速纠正低血糖,血糖水平及生理应答反应(1),血糖水平降低至4.6mmol/l时,胰岛素分泌受抑制血糖水平在3.8mmol/l时，胰高血糖素、肾上腺素开始释放血糖水平在3.0mmol/l时，开始出现低血糖症状血糖水平低于2.8mmol/l时，患者出现进行性认知能力下降血糖低于1.0mmol/l时，患者出现昏迷,血糖水平及生理应答反应(2),低血糖的表现,肾上腺交感神经症状中枢神经症状,肾上腺交感神经症状,低血糖的症状:交感神经和肾上腺髓质兴奋的表现：焦急不安情绪激动手足颤抖、软弱饥饿感心慌出汗面色苍白当血糖降至60ml/dl（3.3mmol/L）以下时就要注意是否出现上述症状。,中枢神经症状,如果血糖低于40mg/dl(2.2mmol/L),就可能出现下述症状：头痛躁动疲倦,可有幻觉意识丧失视物不清语言迟钝神经过敏癫痫发作是由于脑细胞葡萄糖供应不足所致。（通常低血糖发展很快）,中枢神经受抑的表现,血糖下降而持久所致。表现为中枢缺氧缺糖症群，越高级的中枢受抑制越早，恢复越迟。大脑皮层：意志朦胧，头痛头晕，嗜睡，精神失常。皮层下中枢：神志不清，躁动惊厥，瞳孔散大。延脑：昏迷，反射消失，呼吸浅弱，血压下降，瞳孔缩小，历时较久者，不易恢复。混合性：兼有上二种表现，多见。,低血糖的不典型表现,意识障碍合并抽搐，易误诊为癫痫精神症状，烦躁不安，易激惹，情绪激动，语无伦次，有骂人、打人，幻视有时可误诊为脑病及酒精中毒神志清楚，出现肢体，言语障碍，容易误诊为脑血管病昏迷，瞳孔不等大，对光反射迟钝，易误诊为脑疝,低血糖的危害,1型糖尿病患者中至少4%是死于低血糖心血管系统功能神经系统其它：眼睛、肾脏社会活动（学习、就业等）,低血糖影响心血管系统功能,心率增加脉压增加静息期心肌缺血心绞痛心梗,低血糖相关的神经系统损害,低血糖的神经系统损害在有关著作和论文中被作为“神经低血糖”、“低血糖脑病”“低血糖偏瘫”，“低血糖昏迷”，“低血糖危象”，“缺糖性脑病”等等。有人认为为了便于对本病综合征的研究，称做“低血糖的神经系统损害”较为合适,低血糖性脑病可能发病机制,低血糖引起交感神经兴奋而导致脑血管痉挛原有脑动脉硬化的动脉狭窄所引起神经功能损伤低血糖引起神经系统的选择受损,低血糖影响大脑功能,脑干脊髓,Rostrocaudalsensitivitytoneuroglycopenia,脑皮质海马,基底神经节前部丘脑,低血糖对脑损害的Himwich分期,分期症状体征动静脉氧压差EEG,I期：大脑皮质损害II期：脑皮质下间脑损害III期：中脑损害IV期：神经元损害V期：神经元损害及生命中枢损害,定向力下降，吐词不清，嗜睡感觉分辨力丧失，对刺激无反应，但有自主性运动行为，心率快，瞳孔扩大张力性肌强直，眼非同向偏斜，跖反射异常转动头部可诱发四肢的伸肌痉挛昏迷、呼吸弱、心动过缓，眼球固定，瞳孔缩小，无对光反射，体温下降,6.82.61.8,慢波活动增加，节律(814cps)带慢波活动节律(14cps)节律极慢或无脑电波,HimwichHE.In:BrainMetabolismandCerebralDisorders.Baltimore,Williambloodvolumewasinfactincreasedby20%25%,afindingthatisalsosuggestiveofmaximalvasodilatation(seetext).(d)Graphofsingle-oxelMRspectroscopicdatainaffectedrightcerebralcortexshowsdecreasedN-acetylaspartate(NAA)level,preservedcholine(Cho)andcreatine(Cr)levels,andnoevidenceofabnormallactatelevel(arrow1.3ppm).,大脑皮质损害，丘脑未累及,Diffusion-weightedmagneticresonance(MR)imaging(A)andT2-weightedMRimaging(B)showedadiffusecorticalhighsignal.Thebrainstem,cerebellum,andthalamusweresparedaswerethedorsofrontalcortexandoccipitalpoles.Thesignalchangeinthehippocampuswasrelativelysmallondiffusion-weightedMRimaging.OnT2-weightedMRimaging,afocalhigh-signallesionwasseeninthethalamusbilaterally(moreprominentontheleftside)andinthecentrumsemiovale.DiffusewhitematterlesionswereseenontheT2-weightedMRimage,新生儿低血糖MR表现,病例1MRI生后34h出现低血糖表现,58h入院,血糖为1.7mmol/L。AD为生后3d所见。A,B分别为矢状面T1WI和横断面T2WI,可见顶枕叶T1WI低信号,而T2WI改变不明显;C为DWI,可见顶枕叶皮层高信号,提示明显的细胞毒性水肿;DF为生后13dT1WI(D),T2WI(E)和DWI(F)图像,枕部可见明显的T1WI低信号,T2WI高信号,而DWI顶枕部转为低信号,提示皮层发生水肿坏死。,皮质、基底节、脑室旁白质损害,Fig.1ad(Patient5)A57-year-olddiabeticmanwasfoundinacoma6hafterhewaslastseen.Glucoselevelwas16mg/dLatpresentation.Fluid-attenuatedinversionrecoveryimage(a)onthedayofadmissionshowsslightlyincreasedsignalintensityinthecerebralcortexandbasalganglia.Diffusion-weightedimages(b,c)clearlyshowbilaterallysymmetricalhyperintenselesionsinthecerebralcortex,basalganglia,andperiventricularwhitematter(arrows).ADCmap(d)obtainedatthesamelevelascshowscorrespondingreducedADC,内囊、放射冠损害,Figure1.Diffusion-weightedMRIonadmissionshowingthehyperintensitylesionswithinthebilateralinternalcapsule,coronaradiata,andfrontoparietalcortex.Notethatbilateralhippocampidonotdiscloseanyhyperintensitylesions.,Figure2.Diffusion-weightedMRI10daysafterglucoseinfusionshowingregressionofthehyperintensitylesions.,半卵圆中心非对称损害,Fig.5a,b(Patient17)A91-year-olddiabeticmanadmittedfordrowsinessfor10h.Glucoselevelwas24mg/dLatpresentation.Diffusion-weightedimage(a)onthedayofadmissionshowsfocalareaofunilateralhyperintenselesionintheleftcentrumsemiovale(arrows)withreducedADCvalue(b),放射冠、胼胝体损害,Figure1.A,InitialDWI(repetitiontime/echotime/4100/96/90;1000s/mm2;fieldofview230mm;matrix:128128)withincreasedsignalintensitiesinbilateralcoronaradiataandsplenium.B,InitialADCmapswithsignalreductionalsoinbilateralcoronaradiataandspleniumcorrespondingtoDWIimages.,内囊、胼胝体损害,Figure1(A)Diffusion-weightedimaging(DWI)onadmissionshowinghyperintenselesionsinthespleniumofthecorpuscallosumandthebilateralposteriorlimbsoftheinternalcapsules.(B)DWIobtained2hafterglucoseinfusionshowingalmostfullrecoveryexceptforasmallpartofthespleniumofthecorpuscallosum.(C)DWIobtained2daysafterglucoseinfusionshowingcompleteregressionofthehyperintenselesions.,海马、皮质、胼胝体损害,Figure2:Imagesin51-year-oldman(patient2)foundunconscious,withaGlasgowComaScalescoreof7andwithdrawaltopain.(a)Fluid-attenuatedinversionrecoveryand(b)DWMRimagesshowincreasedsignalintensityinthehead,body,andtailofthehippocampusbilaterally(arrowheads)andinthecerebralcortex(arrow).(c)T2-weightedMRimageshowsbilateralpatchyhyperintenselesionsinthecerebralcortex,includingtheinsula(arrow).Thereisalsoinvolvementofthespleniumofthecorpuscallosum(arrowheads).On(d)correspondingDWMRimage,thehyperintenselesionsaremoreprominentthantheyareonc.,胼胝体、脑干损害,Figure4:Imagesin61-year-oldman(patient8)admittedfordrowsiness,confusion,lefthemiparesis,andslurredspeech.(a,b)DWMRimagesshowhyperintenselesionsinthelefthemiponsandthespleniumofthecorpuscallosum.(c,d)RepeatDWMRimagesobtained36hourslatershownochangeinthepontinelesion,butreversalofthecallosalabnormality.,胼胝体、白质弥漫损害,Fig.3ad(Patient14)A32-year-oldwomanwasfoundinacoma2daysaftershewaslastseen.Glucoselevelwas33mg/dLatpresentation.Diffusion-weightedimages(a,b)onthedayofadmissionshowbilaterallysymmetricalconfluenthyperintenselesionsintheperiventricularandsubcorticalwhitematters.Therearealsoinvolvementsofthecorpuscallosumandinternalcapsule.ADCmaps(c,d)atthesamelevelsasaandbshowdecreasedADCintheselesions;thelesionssparedthecorticalanddeepgraymatter,低血糖对眼的影响,低血糖可显著减少玻璃体中的葡萄糖水平加剧缺血视网膜的损伤；严重低血糖可出现眼压突然下降，引起动脉破裂、出血。,低血糖对肾脏的影响,急性