刺激间隔对兔痛觉诱发电位的影响

目的对家兔进行痛刺激间隔与诱发的事件相关电位关系的研究 ,探讨痛刺激间隔对诱发电位的影响 ,筛选兔痛觉诱发电位最优的刺激间隔。方法在家兔颅骨内F4点安放电极 ,用不同的刺激间隔按痛觉Oddball刺激序列记录该部位的波形并对其进行分析。结果痛觉P2、N2、P3a的潜伏期各刺激间隔间无显著性差异 (P >0 5 ) ,波幅在刺激间隔为 8秒时最高 (P <0 0 5 ) ,分别为 ( 63 3 3± 2 5 93 ) μv、( 62 2 5± 13 86) μv、( 5 6 17± 9 82 ) μv。 结论兔痛觉诱发电位有一最佳刺激间隔。     

GABA能递质系统对P3a波的作用及其机制的研究

目的　探讨扣带回及额叶等脑区GABA -A受体 (GABAAR)在P3a波产生中的作用及其相应机制。方法　记录和分析正常状态 (Normal)下以及分别在扣带前回前区 (AcgI)、扣带前回后区 (AcgII)、扣带后回 (Pcg)及背外侧额叶F3(F4 )依次微量注入生理盐水、不同浓度GABAAR拮抗剂Bicuculline及GABA后的ERPs。结果　Bicuculline在AcgI、AcgII、Pcg及F3(F4 )等区对P3a波具有显著不同的作用。但只在AcgI区Bicuculline除使P3a波潜伏期显著延长、波幅降低外 (P <0 .0 1) ,甚至可使P3a波消失 ,外源性GABA使P3a波复现。结论　AcgI区GABAAR的活动与P3a波的产生直接相关。GABAAR介导的IPSP可能是产生P3a波神经化学机制之一。AcgI区GABAAR的活动参与形成P3a波偶极子电穴和 或电源。     

对大白鼠F波性质的初步研究

目的　探讨脊髓后根损伤对F波的影响。方法　 15只Wistar大鼠于窝下游离并刺激坐骨神经 ,在短展肌记录M波与F波 ;将大鼠分为 2组 ,暴露腰脊髓后 ,一组依次切断L3 、L4、L5、L6前根 ;另一组依次切断L3 、L4、L5、L6后根 ,分别观察记录切断前、后根后F波的波幅和潜伏期。结果　切断前根组均表现为F波波幅显著降低 (P <0 .0 1)直至消失 ;切断后根组均表现为F波波幅显著降低 (0 .0 0 1

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听觉 P300电位及其亚成分偶极子分析

目的确定听觉 P300电位及其亚成分 P3a和 P3b波的起源. 方法用听觉 Oddball范式从 15名健康被试者头皮上的 64导电极帽记录事件相关电位( event-related potentials,ERPs),选取 75%总场强( global field power,GFP)的时间范围作为计算偶极子的时间窗,偶极子分析采用逆算法原理. 结果 30%被试者的 P300分叉为 P3a和 P3b波. P300及其亚成分的潜伏期和波幅均具有主效应, P3a电位的潜伏期最短,波幅最小. P300电位的起源可用 1～ 3个等价偶极子表示, P3a及未分叉 P300的前半部分( 240～ 310 ms)的偶极子定位于扣带前回, P3b及未分叉 P300的后半部分( 310～ 420 ms)定位于颞叶内侧附近,包括海马、海马旁回、杏仁核、扣带回及丘脑,未分叉的 P300至少由相当于 P3a和 P3b的两部分组成,并且这两部分的偶极子与 P3a和 P3b的偶极子定位相似. 结论 P300电位中的 P3a亚成分及未分叉 P300前半部分起源于于扣带前回, P3b亚成分及未分叉 P300的后半部分起源于颞叶内侧,包括海马、海马旁回及丘脑等结构.     

听觉P300电位及其亚成分偶极子分析

目的：确定听觉P300电位及其亚成分P3a和P3b波的起源。方法：用听觉Oddball范式从15名健康被试头皮上的64导电极帽记录事件相关电位(event-related potentials，ERPs)，选取75％总场强(global field power．GFP)的时间范围作为计算偶极子的时间窗，偶极子分析采用逆算法原理。结果：30％被试的P300分叉为P3a和P3b波。P300及其亚成分的潜伏期和波幅均具有主效应，P3a电位的潜伏期最短，波幅最小。P300电位的起源可用1-3个等价偶极子表示，P3a及未分叉P300的前半部分(240～310ms)的偶极子定位于扣带前回，P3b及未分叉P300的后半部分(310-420ms)定位于颞叶内侧附近，包括海马、海马旁回、杏仁核、扣带回及丘脑，未分叉的P300至少由相当于P3a和P3b的两部分组成，并且这两部分的偶极子与P3a和P3b的偶极子定位相似。结论：P300电位中的P3a亚成分及未分叉P300前半部分起源于于扣带前回，P3b亚成分及未分叉P300的后半部分起源于颞叶内侧，包括海马、海马旁回及丘脑等结构。     

家兔P300样电位与丘脑腹后外侧核及隔区内侧核关系的研究

目的：研究家兔丘脑腹后外侧核（ＶＰＬ）及隔区内侧核（ＳＥＰ）与Ｐ３００样电位的关系。方法：在家兔颅骨内和ＶＰＬ及ＳＥＰ植入绝缘针电极，记录破坏ＶＰＬ和ＳＥＰ前后颅骨内、ＶＰＬ、ＳＰ的Ｐ３００样电位的变化。结果：破坏ＶＰＬ后头颅所记Ｐ３００样电位无变化。破坏ＳＥＰ后第一天，头颅所记Ｐ３００样电位无变化。第２～６天，头颅所记Ｐ３００样电位Ｐ２７０Ｎ３３０Ｐ４００的潜伏期逐日延长，波幅逐渐降低以至于消失。结论：丘脑腹后外侧核与Ｐ３００的发生毫无关系。ＳＥＰ不是Ｐ３００的起源，但是Ｐ３００电位的存在有赖于ＳＥＰ的完整。Ｐ３ａ的起源可能在ＳＥＰ胆碱能纤维投射的扣带回或嗅皮层。     

胆红素致兔脑瘫动物模型的脑干听觉诱发电位研究

目的：应用脑干听觉诱发电位对胆红素致脑瘫免的听路损害情况进行探讨。方法：对5例脑瘫兔和10例同日龄正常兔的脑干听觉诱发电位进行检测。结果：脑瘫兔组P，波出波率低于正常兔组(P<0.01)；听路损害均呈双侧性．周围性听路损害2只耳，中枢性听路损害3只耳，混合性听路损害5只耳；脑瘫免组P1、P2、P3、P4波潜伏期延长(P<0．01)，P1～P5波幅两组间差异不显(P>0.05)，P1-P2、P1-P4峰间潜伏延长(P<0.01)，P1～P3、P1～P5两组间差异不显(P>0.05)。结论：胆红素致脑瘫兔的脑干听觉诱发电位改变呈双侧性；为蜗后性损害，且以混音性听路损害为主。     

阿尔茨海默病和血管性痴呆的定量脑电图研究

目的探讨阿尔茨海默病(AD)和血管性痴呆(VD)的定量脑电图(QEEG)特征及其与AD、VD患者认知功能的相关性。方法对50例AD患者、50例VD患者及50例健康老年人行脑电图(EEG)功率谱分析。功率谱按频率分为δ波(0.5~3.9Hz)、θ波(4.0~7.9Hz)、α波(8.0~13.9Hz)、β波(14.0~30.0Hz),以(δ+θ)/(α+β)值作为观察评估指标进行比较。对3组EEG异常程度、全脑及FP1、FP2、F3、F4、C3、C4、P3、P4、O1、O2、F7、F8、T3、T4、T5、T6的(δ+θ)/(α+β)值进行比较,并分析其与简明智力状态检查量表(MMSE)评分的相关性。结果AD组中、重度异常EEG发生率明显高于VD组(χ~2=4.11,P0.05)。AD组全脑及FP1、FP2、F3、F4、C3、C4、P3、P4、O1、O2、F7、F8、T3、T4、T5、T6的(δ+θ)/(α+β)值高于对照组,差异均有统计学意义(P0.05)。VD组全脑、FP1、FP2、F4、C3、C4、P4、O1、O2、F7、F8、T3、T4、T5的(δ+θ)/(α+β)值高于对照组,差异均有统计学意义(P0.05)。AD组与VD组各区域(δ+θ)/(α+β)值比较,差异无统计学意义(P0.05)。VD组FP1、F3、C3、F7、T3、T5及全脑左侧的(δ+θ)/(α+β)值均高于右侧对称区域,差异有统计学意义(P0.05)。AD组仅全脑左侧的(δ+θ)/(α+β)值与右侧比较,差异有统计学意义(P0.05);对照组全脑左右侧及各区域左右对称部位的(δ+θ)/(α+β)值比较,差异无统计学意义(P0.05)。AD组、VD组的MMSE评分与各区域(δ+θ)/(α+β)值均呈负相关(P0.05)。结论 QEEG是一种客观、量化的脑功能检测方法,对AD、VD的诊断、鉴别诊断及认知功能评估有重要价值。     

高血钾致室性期前收缩巨大高尖T波1例

1　病例简介患者,男,3岁。乘摩托车翻车时从母亲怀中撞击坠落,当即昏迷。在当地县医院抢救并做头颅CT扫描示:①硬膜外血肿;②颅骨骨折。4h后来我院就诊。查体:T375℃,深昏迷,双侧瞳孔散大(Φ7mm),对光反射消失,无自主呼吸、无心跳。急行心脏按压,气管插管,人工呼吸。1∶10000肾上腺素1mg静推2次,心电、血压监测。5min后自主心率恢复(107次/min),律不齐;血压、意识、自主呼吸均未恢复。甘露醇50mL快速静点,10min后自主呼吸5次/min,极微弱。急描ECG见图1示:窦性P波,PR间期014s,QRS波群呈室上性形态,时间007s,各导联T波高耸尖锐,基底变窄…     

卡片推理与词语结构类比推理对大学生事件相关电位的影响

目的 探讨卡片推理与词语结构类比推理对事件相关电位的影响.方法采用Netsta-tion事件相关电位记录和分析系统,测定14名大学生的事件相关电位.结果 4卡片推理与类比推理在头皮前部和后部正确反应和错误反应,波幅差异不均衡;150 ms-300 ms时窗下,反应类型和记录点的交互作用显著(F=1.838,P<0.05);记录点的主效应显著(F-1.874,P<0.05);250 ms-500 ms时窗下,记录点的主效应显著(F=2.516,P<0.05).结论 4卡片条件推理与类比推理具有不同的神经机制,大脑左半球和右半球在两种推理中起着不同的作用.     

P3a电位神经学起源的实验研究

目的　研究P3a电位神经起源之所在。方法　以家兔为实验对象,记录额叶、扣带前回和扣带后回损毁前后的P3a电位。结果　P3a极性反转者仅见于扣带前回;损毁扣带后回,P3a波幅及潜伏期无改变;损毁额叶,P3a波幅及潜伏期无显著性改变;同时损毁额叶和扣带前回,P3a消失或波幅降低。结论　扣带前回与P3a发生有关。     

穿梭硬膜悬吊法和常规硬膜悬吊法在颅骨修补术中应用的对照研究

目的 通过穿梭硬膜悬吊和常规硬膜悬吊在颅骨修补术中的对照研究,探讨“穿梭”缝合硬膜悬吊法在颅骨修补术中的应用价值.方法 回顾性分析62例采用数字化三维塑形钛网修补的颅骨缺损患者的资料.按其硬膜悬吊方法的不同,分为常规硬膜悬吊组24例和穿梭缝合硬膜悬吊组38例.对两组的手术时间、住院时间和并发症进行分析.结果 穿梭硬膜悬吊组手术时间（95.80±17.31） min短于常规组[（105.41±14.62） min];住院时间（11.60±0.82）d,少于常规组[（13.00±2.54）d];两组比较差异均有统计学意义（t值分别为2.270、3.426,P均＜0.05）.穿梭组并发症发生率为3％（1/38）,明显低于常规组[25％ （6/24）],两组比较差异有统计学意义（P=0.011）.结论 穿梭缝合硬膜悬吊法能够缩短手术时间和住院时间,降低手术并发症的发生率,值得临床应用.     

硬脊膜完整性可影响脑脊液中细胞因子的水平

背景：脊髓损伤后的病理生理机制非常复杂,人们对此认识还很不全面、深入。目的：观察脊髓损伤动物模型中硬脊膜完整性对脑脊液内细胞因子水平的影响。方法：采用钳夹压迫法建立新西兰大白兔脊髓损伤模型,随机分为无硬脊膜缺损组、硬脊膜缺损组、硬脊膜缺损复合膜修复组、硬脊膜缺损自体筋膜修复组。术后 30 min、1 h、3 h、6 h、12 h、36 h 采用酶联免疫吸附实验方法检测各组脑脊液中细胞因子白细胞介素 6、白细胞介素 10、肿瘤坏死因子α的变化。结果与结论：无硬脊膜缺损组、硬脊膜缺损复合膜修复组和硬脊膜缺损自体筋膜修复组术后 6 h 脑脊液中白细胞介素 6、白细胞介素 10、肿瘤坏死因子α水平均显著低于硬脊膜缺损组（P 〈 0.05）。其余时间点 4 组间各因子水平差异无显著性意义（P 〉 0.05）。说明维护脊髓损伤模型中硬脊膜的完整性可影响脑脊液中白细胞介素6、白细胞介素 10、肿瘤坏死因子α水平,抑制炎症反应。     

Influence of Polarity Reversal on de-fibrillation Success with Biphasic Shocks and a Transvenous/Subcutaneous Defibrillator System in a Porcine Animal Model

Clinical studies show that polarity reversal affects de-fibrillation success in transvenous monophasic defibrillators. Current devices use biphasic shocks for de-fibrillation. We investigated in a porcine animal model whether polarity reversal influences de-fibrillation success with biphasic shocks. In nine anesthetized, ventilated pigs, the de-fibrillation efficacy of biphasic shocks (14.3 ms and 10.8 ms pulse duration) with “initial polarity” (IP, distal electrode = cathode) and “reversed polarity” (RP, distal electrode = anode) delivered via a transvenous/subcutaneous lead system was compared. Voltage and current of each defibrillating pulse were recorded on an oscilloscope and impedance calculated as voltage divided by current. Cumulative de-fibrillation success was significantly higher for RP than for IP for both pulse durations (55% vs 44%, P = 0.019) for 14.3 ms (57% vs 45%, P < 0.05) and insignificantly higher for 10.8 ms (52% vs 42%, P = n.s.). Impedance was significantly lower with RP at the trailing edge of pulse 1 (IP: 44 ± 8.4 vs RP: 37 ± 9.3 with 14.3 ms, P < 0.001 and IP: 44 ± 6.2 vs RP: 41 ± 7.6 Ω with 10.8 ms, P < 0.001) and the leading edge of pulse 2 (IP: 37 ± 5 vs RP: 35 ± 4.2 Ω with 14.3 ms, P = 0.05 and IP: 37.5 ± 3.7 vs RP: 36 ± 5 Ω with 10.8 ms, P = 0.02). In conclusion, in this animal model, internal de-fibrillation using the distal coil as anode results in higher de-fibrillation efficacy than using the distal coil as cathode. Calculated impedances show different courses throughout the shock pulses suggesting differences in current flow during the shock.     

Polarity Reversal Improves Defibrillation Efficacy in Patients Undergoing Transvenous Cardioverter Defibrillator Implantation with Biphasic Sbocks

The purpose of this study was to determine the influence of polarity reversal on DFT in patients undergoing implantation of nonthoracotomy defibrillators with biphasic shocks. Previous studies have shown higher defibrillation efficacy with using the distal electrode as anode in implantation of nonthoracotomy defibrillators and monophasic shocks. However, it is as yet unclear whether biphasic shock defibrillation will also be influenced by polarity reversal. Using a transvenous lead system with a proximal electrode in the superior caval vein and a distal electrode in the RV apex, 27 patients undergoing defibrillator implantation were randomized to DFT testing with "initial" (distal electrode = cathode) or "reversed" polarity (distal electrode = anode). Defibrillation energy was reduced stepwise until defibrillation failure occurred. At this point, polarity was switched and testing continued until the lowest energy requirement was determined for both polarities. With reversed polarity, DFT was 11.1 ± 5.7 J versus 13.3 ± 5.8 J with initial polarity (P = 0.033). This means a 17% reduction of the DFT. In 10 patients, the threshold was lower with reversed, whereas in 3 patients it was lower with initial polarity. In conclusion, changing electrode polarity in transvenous implantable defibrillators with biphasic shocks may significantly influence defibrillation energy requirements. Therefore, polarity reversal should always be attempted before considering patch implantation.     

Optimized Pulse Durations Minimize the Effect of Polarity Reversal on Defibrillation Efficacy with Biphasic Shocks

There are conflicting results on the effect of polarity change on the defibrillation efficacy of biphasic shocks possibly caused by different shock durations. The goal of the present study was to investigate the influence of polarity reversal on defibrillation efficacy for different biphasic shock durations in a porcine animal model. In eight anesthesized pigs using a transvenous/submuscular lead system DFTs for 4 phase 1 durations were determined: 8.1 ms, 6 ms, 3.8 ms and 1.7 ms. The phase 1/phase 2 ratio was constant at 60%/40%. For cathodal shocks, the defibrillation coil in the right ventricular apex was the cathode during phase 1 and for anodal shocks it was the anode. For both polarities, the strength-duration curve revealed a DFT minimum at 3.8 ms (cathodal shocks: 21.3 +/- 6.4 J, P < 0.001; anodal shocks: 21.9 +/- 8 J, P = 0.05). For anodal shocks and phase 1 durations of 1.7, 3.8, and 6 ms there was no significant difference of the stored energy at the DFT compared to cathodal shocks. In contrast, significantly lower DFTs were observed for anodal shocks with a phase 1 duration of 8.1 ms (28.8 +/- 6.4 J compared to 33.1 +/- 5.9 J for cathodal shocks, P = 0.006). The effect of lower defibrillation energy requirements with polarity reversal depends on the total biphasic shock duration; for the pulse duration with the lowest DFT, polarity reversal does not increase defibrillation efficacy of biphasic shocks.     

Adaptation of rabbit cortical collecting duct HCO3- transport to metabolic acidosis in vitro.

Net HCO3- transport in the rabbit kidney cortical collecting duct (CCD) is mediated by simultaneous H+ secretion and HCO3- secretion, most likely occurring in a alpha- and beta-intercalated cells (ICs), respectively. The polarity of net HCO3- transport is shifted from secretion to absorption after metabolic acidosis or acid incubation of the CCD. We investigated this adaptation by measuring net HCO3- flux before and after incubating CCDs 1 h at pH 6.8 followed by 2 h at pH 7.4. Acid incubation always reversed HCO3- flux from net secretion to absorption, whereas incubation for 3 h at pH 7.4 did not. Inhibition of alpha-IC function (bath CL- removal or DIDS, luminal bafilomycin) stimulated net HCO3- secretion by approximately 2 pmol/min per mm before acid incubation, whereas after incubation these agents inhibited net HCO3- absorption by approximately 5 pmol/min per mm. Inhibition of beta-IC function (luminal Cl- removal) inhibited HCO3- secretion by approximately 9 pmol/min per mm before incubation, whereas after incubation HCO3- absorption by only 3 pmol/min per mm. After acid incubation, luminal SCH28080 inhibited HCO3- absorption by only 5-15% vs the circa 90% inhibitory effect of bafilomycin. In outer CCDs, which contain fewer alpha-ICs than midcortical segments, the reversal in polarity of HCO3- flux was blunted after acid incubation. We conclude that the CCD adapts to low pH in vitro by downregulation HCO3- secretion in beta-ICs via decreased apical CL-/base exchang activity and upregulating HCO3- absorption in alpha-ICs via increased apical H+ -ATPase and basolateral CL-/base exchange activities. Whether or not there is a reversal of IC polarity or recruitment of gamma-ICs in this adaptation remains to be established.     

颅骨生长性骨折的病理学基础和临床X线研究

本文报告１０例生长性颅骨骨折，对该病的形成机理、病理学基础、Ｘ线表现及其类型进行了探讨。该病的特征为骨折多见于额骨和顶骨，多发生于颅骨生长的活跃期，在骨折同时伴有硬脑膜和蛛网膜的破裂，随后硬脑膜缺损，骨折扩大形成一个颅骨缺损，伴随着骨折下方脑的挫伤和局限性脑肿胀，常致使头部局限性包块形成。局限性大脑损害可导致一组晚期的病理学后遗症改变包括：局限性脑萎缩、脑穿通或囊肿、局限性脑室扩大以及复杂的疤痕可累及硬脑膜、软脑膜、蛛网膜和大脑。除此之外，我们认为颅骨下硬脑膜的分离和局部缺血也可是颅骨生长性骨折的原因之一。     

硬脑膜分层脑膜成形术的应用研究

目的:为了解决开颅手术后硬脑膜无法缝合而造成的脑组织与头皮下组织的粘连以及可能发生脑脊液漏等并发症。方法:设计硬脑膜分层脑膜成形术,将硬脑膜人为地分为二层,使其面积扩大一倍,经过成形裁剪,可完整修复硬脑膜并形成较宽松的硬膜下腔。结果:11例12人次使用硬脑膜分层成形术。(1)很松弛地关闭了硬脑膜,保护了脑组织,无一例发生脑脊液漏和癫痫;(2)术后硬脑膜松弛有1 cm提高范围;(3)6例术后三月再行颅骨修补术,全部顺利完成手术,术中切开硬脑膜证实硬膜与脑组织无粘连。结论:硬脑膜分层成形术是解决术后颅压高致硬脑膜不能缝合的新办法,具有简便、经济实用、无排异反应可防止脑粘连并发症的优点。特别适合于农村合作医疗工作的推广应用。