蟾蜍坐骨神经复合动作电位相对不应期的特征

背景：神经纤维疾病的患者经常被推荐做复合动作电位相对不应期的测定，但其在不同刺激条件下的特性始终并未完全证实。目的：通过蟾蜍坐骨神经复合动作电位的实验，更加全面地阐述复合动作电位相对不应期爆发动作电位的特点。设计：随机非对照的实验研究。地点和对象：由首都医科大学实验动物中心提供的6只蟾蜍，在同一生理学实验室被处死来做实验。干预：以不同的刺激强度和组合方式刺激神经。主要观察指标：用NSA-Ⅲ医学信号处理系统记录相对不应期发生动作电位的幅度。结果：在相对不应期的同一时刻，较强的刺激会引起较大幅度的复合动作电位，并且在同样的刺激强度下，不会产生太大变化。结论：在同一时期对相对不应期的刺激可引起不同阈值的神经纤维不同概率性的兴奋，但它们可以固定的概率性叠加，以形成稳定的动作电位。此外，神经干中A类神经纤维的最短绝对不应期可以通过足够强的刺激来测定。     

大脑经颅磁刺激的疼痛治疗研究指南

<正>1.经颅磁刺激原则和应用在1985年,经颅磁刺激(transcranial magnetic stimulation,TMS)首次被证实以电磁感应能够引起周围细胞的电效应。一定强度的TMS作用可以充分地使神经细胞去极化产生动作电位。低强度的TMS可以几乎达到抑制性中间神经元的阈值,而更高强度的刺激则兴奋神经元。(1)对侵入性脑刺激治疗疼痛研究的思考运动皮层电刺激(motor cortexstimulation,MCS)     

同一手不同手指的复合感觉神经动作电位比较

逆行复合感觉神经动作电位（compoundsen sory nerve action potentials，CSNAPs）是高于刺激手指而记录到的顺行CSNAPs。在临床神经生理学实验中。CSNAPs的幅度和传导速度（CVs）是决定神经传导功能的重要测量手段．相对于CVs来说，CSNAPs的绝对值在个体中更多变．甚至在同一个体中。非优势手与优势手比较，其CSNAPs相对较高。     

重新评价刺激掌正中神经返支诊断腕正中神经失用症

<正> 神经失用症是指神经结构完好但传导功能障碍。如果去除导致传导阻滞的原因,那么神经的传导功能可以恢复。本研究的目的是观察刺激掌正中神经返支(recurrent mediannerve,RMN)引发的尺深神经(deep ulnar nerve,DUN)兴奋的可能性,并确定在刺激掌以后DUN活动和肌肉复合动作电位幅度增加之间的关系。     

双向脉冲可实现的神经纤维选择性兴奋

背景：研究证明利用电刺激外周神经纤维可恢复一些因失去中枢神经控制的肌肉的功能。目的：验证双电极 1 mm 较近距离下双向方波脉冲实现神经选择性兴奋的正确性,并基于此实现神经的选择性兴奋。方法：成年 Wistar 大鼠 8 只,麻醉后暴露大鼠坐骨神经,将电极小心放于坐骨神经干,建立神经选择性刺激模型。实验用电极为自制 Cuff 双极性电极,刺激器采用的是 Grass S88 刺激器和 AWG2005 任意波形信号发生器。采取双电极双向刺激方式,两个电极之间距离为 1 mm,刺激波形选用脉宽为 0.2 ms 的对称双向脉冲,其输出脉冲的幅度、脉宽和延时均可调。调节刺激强度,研究双电极双向刺激下神经兴奋性的规律,以此实现神经的选择性兴奋,并利用＂碰撞法＂原理验证利用双电极双向刺激方法实现神经选择性兴奋的可行性。结果与结论：实验过程中神经动作电位的变化将经 P511 放大器放大后接入示波器显示,双电极刺激波形为脉宽为 0.2 ms 的对称双向脉冲。随着刺激幅度的增大,实现神经的选择性兴奋。说明用距离很近（1 mm）的双电极双向对称脉冲的方法实现了神经的选择性兴奋,并利用＂碰撞法＂原理证实了此种方法的有效性和可行性。     

碱性成纤维细胞生长因子复合缓释降解膜对同种异体移植神经的影响：电生理评价

目的:应用电生理检测指标评价碱性成纤维细胞生长因子复合缓释降解膜对周围神经再生的影响。方法:实验于2005-03/11在沈阳医学院奉天医院实验室完成。①实验材料:碱性成纤维细胞生长因子复合缓释降解膜:主要成分为碱性成纤维细胞生长因子、维生素C抑制剂、明胶、壳聚糖。②实验分组:大耳白兔60只,按随机数字表法分为实验组和对照组,每组30只。异体正中神经制备:每组兔分6次取正中神经,每次取5只兔的正中神经,分别切除双侧正中神经各2.5cm,用受体动物血浆浸泡20min、-196℃液氮冷存21d、室温下复温。手术方法:麻醉后暴露双侧上臂正中神经主干,在相应一致神经部位切除2.5cm,用复温后的异体正中神经缝接。实验组神经缝接处包裹碱性成纤维细胞生长因子复合缓释降解膜,对照组不包膜。③实验评估:术后8,13,26周采用Keypoint肌电诱发电位仪测定运动神经传导速度和复合肌肉动作电位波幅。采用Luzex-F图像分析仪测定移植神经近段和远段的锇酸髓鞘染色横断面标本上有髓神经纤维数量。结果:①运动神经传导速度:术后8,13,26周实验组运动神经传导速度明显快于对照组[分别为(21.62±2.81),(13.16±1.81)m/s;(40.83±3.66),(21.71±2.40)m/s;(50.41±4.84),(31.96±3.17)m/s],两组间差异有非常显著性意义(t=3.51,3.69,3.88,P<0.001)。②复合肌肉动作电位波幅:术后8,13,26周实验组复合肌肉动作电位波幅则明显高于对照组[分别为(1.47±0.16),(0.83±0.07)mV;(4.82±1.27),(2.66±0.31)mV;(14.55±4.16),(8.63±3.36)mV],两组间差异有显著性意义(t=2.34,2.48,2.66,P<0.05)。③有髓神经纤维数量:实验组术后13周神经近段和远段有髓神经纤维比例为2.5∶1,术后26周比例为1.2∶1;而对照组相应时间点有髓神经纤维比例分别为7.2∶1和2.2∶1。结论:神经传导速度和复合肌肉动作电位波幅检测结果提示碱性成纤维细胞生长因子复合缓释降解膜有促进周围神经再生的作用。     

磁线圈刺激臂丛的方法

<正> 对臂丛损伤的传统电诊断评价只能靠肌电图。通常在Erb's点采用两个皮肤电极,刺激强度在20mm深处损失95％～96％;40mm深处损失99％。如果以增加刺激强度来补偿这种损失,又受到仪器容量和产生不必要疼痛的限制。也常难记录到。磁线圈刺激提供了一个刺激外周神经的无痛性方法。变化的磁场可引起神经的去极化,发放动作电位沿神经传导,其作用如同电刺激一样。在深处神经,刺激强度的降落较电刺激大为减少。在20mm深处损失     

基于实验数据计算机仿真大鼠视神经纤维对于胞外点电极刺激的响应与影响

背景:目前的视觉假体有3种,即视网膜假体,视神经假体和视觉皮质假体,保证视神经纤维的正常是使用视神经假体的基础.对于有髓视神经纤维的胞外刺激实际上是胞内刺激的延续和发展,与胞内刺激相比,胞外刺激的优势在于刺激位置的选择更加灵活,操作上的精确度要求相对较低.目的:通过计算机来仿真大鼠视神经纤维对于胞外点电极源刺激的响应,然后考虑电极位置对响应的影响.方法:总结大鼠视神经的实验数据和常见离子通道的特性,分析已有的类Hodgkin-Huyley视神经纤维模型;然后用计算机仿真出神经纤维模型的响应;通过改变胞外点电极源的刺激位置,比较视神经纤维各Ranvier节动作电位的变化.结果与结论:利用模型仿真说明胞外电极位置对视神经响应有影响.点电极源与视神经纤维的垂直距离越近,并且与视神经纤维中心Ranvier节点的水平距离越近,视神经纤维越容易兴奋.     

微波促进大鼠面神经机械性损伤的修复作用

目的:探讨面神经机械损伤后微波的促修复作用。方法:实验于2003-10在复旦大学附属华山医院完成。选择SD雄性大鼠36只,制备右侧面神经损伤模型后随机分为微波组和对照组。微波组又分为术后1,2,4周,每组8只,接受1,2,4周的微波短期照射。对照组同样分成术后1,2,4周3组,每组4只,不接受微波照射。两组大鼠于各时间点行面神经复合肌动作电位检查和组织病理学观察。结果:微波组由于造模失败死亡4只,最终有32只大鼠进入结果分析。①术后1周,微波组、对照组刺激面神经均未能引起面肌的兴奋;术后2周,两组面神经复合肌动作电位潜伏期均有延长,但两组差异无显著性意义;术后4周,微波组刺激面神经引发的面神经复合肌动作电位潜伏期低于对照组[(1.53±0.06),(3.43±0.78)ms,P<0.05]。②光镜观察下,微波组神经束内新生小血管明显多于对照组,神经纤维变性坏死形成空泡明显少于对照组。结论:微波照射可降低损伤面神经的复合肌动作电位潜伏期,起到促进面神经轴突再生作用,从而说明微波对面神经损伤修复具有促进作用。     

关于H反射波幅的新评价指标和临床应用研究进展

<正>H反射是一种可以在人类记录到的非侵入性的简单反射,类似脊髓牵张反射但又不完全等同于牵张反射~([1]),可以用于脊髓Ia反射弧通道、脊髓兴奋环路、定量运动神经元池兴奋性等方面的研究~([2—3])。H反射的产生是通过电流刺激混合神经的传入纤维,其产生的神经冲动主要通过脊髓的单突触反射到同侧运动神经元池,引起运动神经元募集产生复合肌肉动作电位~([4])。H反射的波幅可以反映给定刺激强度下反射所激活的运动单元数量,在一定条件下H反射波幅的改变还     

Mechanoelectrical feedback: independent role of preload and contractility in modulation of canine ventricular excitability.

Mechanoelectrical feedback, defined as changes in mechanical state that precede and alter transmembrane potential, may have potential importance in understanding the role of altered load and contractility in the initiation and modulation of ventricular arrhythmias. To assess the independent effects of preload and contractility on myocardial excitability and action potential duration, we determined the stimulus strength-interval relationship and recorded monophasic action potentials in isolated canine left ventricles contracting isovolumically. The strength-interval relationship was characterized by three parameters: threshold excitability, relative refractory period, and absolute refractory period. The effects of a threefold increase in left ventricular volume or twofold increase in contractility on these parameters were independently assessed. An increase in preload did not change threshold excitability in 11 ventricles but significantly shortened the absolute refractory period from 205 +/- 15 to 191 +/- 14 ms (P less than 0.001) (mean +/- SD). Similarly, the relative refractory period decreased from 220 +/- 18 to 208 +/- 19 ms (P less than 0.002). Comparable results were observed when contractility was increased as a result of dobutamine infusion in 10 ventricles. That is, threshold excitability was unchanged but the absolute refractory period decreased from 206 +/- 14 to 181 +/- 9 ms (P less than 0.003), and the relative refractory period decreased from 225 +/- 17 to 205 +/- 18 ms (P less than 0.003). Similar results were obtained when contractility was increased with CaCl2, indicating that contractility associated changes were independent of beta-adrenergic receptor stimulation. An increase in preload or contractility was associated with shortening of the action potential. A threefold increase in preload and twofold increase in contractility were associated with a decrease in action potential duration of 22 and 24 ms, respectively. There was a significant linear correlation between action potential duration and excitability (absolute refractory period). The similar effects of increased preload and contractility on threshold excitability and refractoriness can be explained by the action these perturbations have on the time course of repolarization. Therefore, excitability of the ventricle is sensitive to and is modulated by alteration of load or inotropic state. The similar effects of either increased preload or contractility on excitability may be mediated by a common cellular mechanism which results in a rise in intracellular free Ca2+ and secondary abbreviation of the action potential.     

Differential effects of stimulus intensity on peripheral and neuromagnetic cortical responses to median nerve stimulation

To study the differential effects of tactile stimulus intensity on cortical and peripheral responses, we measured neuromagnetic cortical responses, compound muscle action potentials (CMAP), sensory nerve action potentials (SNAP), and the subjective estimation of tactile magnitude to electric median nerve stimulation at the wrist in 13 male healthy adults. The sensory perception threshold (ST) for electric pulses at wrist skin was determined and then various levels of stimulus intensity (1 approximately 6 ST) were given to each subject. At 1 ST, only the P50m components of the primary somatosensory (SI) cortical responses were recorded. The second somatosensory (SII) cortical responses were saturated at 2 ST, while the SI responses reached maximum at 3 ST equivalent to the subjective threshold intensity for "strong" tactility. The CMAP and SNAP were maximum at 4-5 ST. At 2 ST, >70% of maximum SI responses were produced, whereas only <40% of maximum CMAP or SNAP responses were obtained. We concluded that the stimulus intensities for activating or saturating somatosensory cortical responses were lower than those for CMAP and SNAP. The differential intensity effects on cortical and peripheral responses suggest a polysynaptic organization underlying the central amplification for somatosensory cortical activation. The optimal intensity levels for producing maximum SI and SII responses were 3 and 2 ST, respectively. Compared with the SII, the SI plays a crucial role in the coding of the tactile stimulus intensity.     

Acute effects of lidocaine on repolarization and conduction in patients with coronary artery disease

Right ventricular repolarization and refractoriness were studied during continuous infusion of lidocaine in patients with coronary artery disease. Compared with baseline the duration of monophasic action potential was shortened (p less than 0.01) at constant and premature stimulation. Early premature action potentials were less shortened (p less than 0.05). Therefore the difference between the longest and shortest action potential duration elicited 2 to 150 msec after refractoriness decreased during lidocaine infusion (p less than 0.01). The right ventricular effective refractory period was shortened similarly to the action potential duration. Lidocaine did not change the conduction of constant paced beats, whereas the more rapid conduction of the midrange premature beats was inhibited (p less than 0.01). The inhibition of premature conduction 50 to 150 msec from the right ventricular effective refractory period may be attributed to the effect of lidocaine on the rate-dependent recovery from inactivation. The effect on the restitution curve indicates that lidocaine may influence the dispersion of premature action potentials in human beings.     

Compound nerve action potential of common peroneal nerve recorded at fibular neck: its clinical usefulness

OBJECTIVE: To determine the clinical usefulness of the compound nerve action potential of the common peroneal nerve recorded immediately distal to or at the fibular neck, at the same time stimulating the common peroneal nerve laterally at the posterior knee. DESIGN: For recording the compound nerve action potential of the common peroneal nerve, the active recording electrode was secured just distal to or at the fibular neck area, whereas the stimulating electrode was placed on the medial border of the lateral hamstring tendon at the level of the popliteal crease. To reduce shock artifacts, a biphasic stimulation was used. RESULTS: In 35 adults (n = 19 men), 70 nerves were tested. The compound nerve action potential from each individual was recorded. The compound nerve action potential amplitude of a baseline-to-negative peak and conduction velocity were measured on both sides. For comparisons of the side-to-side amplitude and conduction velocity, Wilcoxon's signed-rank test was applied. CONCLUSION: This approach of recording the compound nerve action potential of the common peroneal nerve, in addition to conventional methods, may enhance the process of determining the precise localization of peroneal nerve lesion in the knee.     

Ulnar nerve entrapment at the elbow localized by short segment stimulation

The purpose of the study was to evaluate the differences in the amplitudes of the compound muscle action potentials of the hypothenar muscles and the differences in conduction times. Differences in shoot segment responses were determined by stimulating the ulnar nerve at 2-cm intervals across the elbow in 20 normal adults. Thirteen ulnar nerves on the left side and 12 nerves on the right of 14 men and six women were studied for motor nerve conduction velocity. The amplitudes of the hypothenar compound muscle action potentials and the conduction times after supramaximal stimulation of the ulnar nerve were also determined. The distal-to-proximal reduction in the amplitude of the potentials was 6% on the left and 4.2% on the right. The maximum conduction time in a 2-cm segment on the right side was 0.63msec (mean +2SD = 0.43 + 0.20) and on the left, 0.60msec (mean +2SD = 0.44 + 0.16). Using the same short segment stimulation technique, ulnar nerve motor conduction was also studied in 13 patients with suspected ulnar neuropathy at the elbow in order to localize the nerve lesion. Conduction time only was abnormal in one patient, both conduction time and amplitude in nine, amplitude only in one, and conduction time and mild reduction in amplitude in two. It was concluded that short segment stimulation of the ulnar nerve at the elbow is useful in localizing the exact site of entrapment/compression of the nerve at the elbow.     

周围神经干的超声定位

目的观察周围神经干超声声像图结构特征,并验证超声引导穿刺定位神经干的准确性。方法对20例志愿者行肌皮神经、坐骨神经、胫神经超声检查,对其中6位志愿者行肌皮神经穿刺定位,5位志愿者行胫神经穿刺定位,9例志愿者行坐骨神经穿刺定位。结果20例志愿者均有效显示相应神经干,肌皮神经、胫神经及坐骨神经显示率为100%。横断面上周围神经干内部呈低回声,周边见膜状高回声的筛孔状结构,纵切面上表现为中等回声,内见线性平行回声的管状结构。6例肌皮神经及5例胫神经超声引导穿刺定位均一次性成功,电刺激验证神经定位准确,引起相应肌肉收缩的电流强度分别为0～0.4mA及0.2～1.0mA,9例坐骨神经超声引导穿刺定位一次性成功7例,二次穿刺定位成功2例,电刺激验证神经定位准确,引起相应肌肉收缩的电流强度分别为0.2～1.4mA。结论超声能清晰显示周围神经干的走行及结构特征,并能准确定位。     

Characterization of the class I antiarrhythmic activity of cibenzoline succinate in guinea pig papillary muscle

The effects of cibenzoline on transmembrane action potentials were examined in guinea pig papillary muscle. Cibenzoline (1-128 microM) did not alter the action potential durations at 50 and 90% of repolarization, the effective refractory period or the ratio of effective refractory period to action potential duration at 90% of repolarization. Likewise, the maximum diastolic potential was virtually unaffected. Cibenzoline depressed the maximum rate of rise of phase 0 (dV/dtmax). This effect was dependent on the rate of stimulation and occurred at a relatively low concentration (2 microM). The onset of use-dependent depression was monoexponential and dependent on the drug concentration, as well as the rate of stimulation. The rate of recovery from use-dependent depression also followed a single exponential time course but was independent of drug concentration and stimulation rate. When cibenzoline and lidocaine were combined in the tissue bath, dV/dtmax recovered with a double exponential time course. The first and second components of this recovery corresponded to the time course observed with lidocaine (first) and cibenzoline (second) alone. Also, the magnitude of the second component was less with the combination than with cibenzoline alone, indicating an interaction between the two drugs. In addition, cibenzoline shifted the curve relating normalized dV/dtmax to membrane potential in the hyperpolarizing direction. Finally, cibenzoline did not alter slow-response action potentials induced by elevated [K]o and isoproterenol. The authors conclude that cibenzoline acts as a class la antiarrhythmic agent in guinea pig papillary muscle.     

Suppression of motor evoked potentials in a hand muscle following prolonged painful stimulation.

Earlier investigations have shown that stimulation of peripheral afferent nerves induces prolonged changes in the excitability of the human motor cortex. The present study compared the effect of experimental pain and non-painful conditioning stimulation on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in the relaxed first dorsal interosseous (FDI) and flexor carpi ulnaris (FCU) muscles. The MEPs were measured in 10 healthy subjects, and stimulus-response curves were generated before and after each of four stimulation paradigms conducted in random order on separate occasions: (a) control; (b) "dual stimulation" consisting of electrical stimulation of the FDI motor point paired with TMS; (c) painful infusion of hypertonic saline in the FDI muscle; and (d) pain combined with dual stimulation. There were no significant changes in FDI MEPs following the control paradigm, and dual stimulation induced an increase in the FDI MEPs only inconsistently. In contrast, the painful stimulation and the combined pain and dual stimulation paradigms were followed by significant suppression of the FDI MEPs at higher stimulus intensities. No changes were observed in the FCU MEPs following the four paradigms. In two additional subjects, the responses evoked in FDI by direct stimulation of the descending corticospinal tracts were significantly depressed following painful stimulation of the FDI, although the ulnar-evoked M-waves remained constant. It is concluded that muscle pain is followed by a period with profound depression of MEPs amplitudes in the resting muscle, but that these changes are at least in part due to a lasting depression of the excitability of the motoneurones in the spinal cord. Hence, painful stimulation differs from non-painful, repetitive stimulation, which facilitates the corticomotor pathway.     

Long-term changes in sciatic-evoked A-fiber dorsal horn field potentials accompany loose ligation of the sciatic nerve in rats

The goal of the present study was to examine whether loose ligation of the sciatic nerve was associated with long-term changes in neuronal excitability in the spinal dorsal horn in urethane-anesthetized rats. The sciatic nerve was stimulated with 0. 1 ms long pulses at 1 stimulus/5 min, and the evoked dorsal horn field potentials remained stable in the absence of tetanic stimulation. In one set of control and ligated animals, high-frequency tetanic stimulation was applied to the nerve at 50 Hz (one 400 ms train of twenty 0.1 ms pulses), and the field potentials were recorded again (1 stimulus/5 min) for up to 4 h post-tetanus. In control animals, this protocol produced significant increases in field potential amplitudes at 15, 30 and 60 min post-tetanus. Interestingly, after this time the evoked field potentials began to decrease, and attained less than 50% of their pre-tetanic values at 240 min post-tetanus. In contrast, in ligated rats the pattern of post-tetanic potentiation was significantly different as the increases in amplitude persisted, and at 240 min post-tetanus the field potentials were almost twice their baseline values.In another set of control and ligated animals, low-frequency tetanic stimulation was applied at 5 Hz (one 400 ms train of two 0.1 ms pulses). Again a differential pattern of post-tetanic responses between control and ligated rats was seen. In control animals, a significant decrease in amplitude was evident within 30 min, and the depression became progressively more pronounced as the field potentials attained about a quarter of their baseline values at 180 min, and remained at these low levels at 240 min post-tetanus. On the other hand, in ligated animals, the depression was not significant, and at 240 min post-tetanus the field potentials were still at about 80% of their baseline values.These data demonstrate that long-term changes in spinal dorsal horn neuronal excitability accompany sciatic ligation to perhaps contribute to the development of neuropathic pain. These changes may result from a lessening of normally strong inhibitory processes in the spinal dorsal horn to generate conditions which favor post-tetanic potentiation over depression of dorsal horn neuronal responses.     

Changes in nerve conduction and Pi/PCr ratio during denervation-reinnervation of the gastrocsoleus muscles of rats.

The purpose of this investigation was to study the changes in nerve conduction and phosphate metabolites of the gastrocsoleus muscles of rats during denervation-reinnervation. Sixteen male Sprague-Dawley rats underwent unilateral crush-denervation of the left sciatic nerves at the sciatic notch. Six rats were used for measurement of motor conduction latency and action potential amplitude of the gastrocsoleus muscle by stimulating the sciatic nerve at one, two and eight weeks after nerve crush. The other ten rats were designated for evaluation of the ratio of inorganic phosphorous (Pi) to phosphocreatine (PCr) by a 31P-phosphoenergetic spectrometer at two weeks and eight weeks after nerve crush. None of the sciatic nerves showed conduction to the gastrocsoleus at one or two weeks after nerve crush. At eight weeks postcrush, the motor conduction latency returned to within normal limits, whereas the action potential amplitude was only 55% of the normal. For the eight-week period of study, the Pi/PCr ratio of the normal control muscles ranged between 0.09 +/- 0.02 and 0.11 +/- 0.02 (mean +/- SD). The denervated muscles showed an increase of Pi/PCr ratio by 54% at two weeks postcrush, compared to the respective contralateral control sides. The ratios returned to the normal value by eight weeks postcrush. In summary, these data suggested that the metabolic recovery of the crush-denervated muscle followed the same pattern as the parameters of nerve conduction.