经皮电刺激诱发肌电潜伏期与身高的关系

本文应用高电压、低输出阻抗刺激器,经皮给予人大脑皮层和脊髓电刺激,同时在上肢鱼际和下肢胫骨前肌记录诱发肌肉动作电位,并测定其刺激大脑皮层所诱发反应的潜伏期－皮层潜伏期、刺激脊髓所诱发反应的潜伏期－脊髓潜伏期。结果表明：皮层潜伏期（Ｌｃｏｒ．）和脊髓潜伏期（Ｌｓｐ．）与身高呈正相关,相关系数是：鱼际：ｒＬｃｏｒ．＝０．２０８,ｐ＜０．０５（ｖ＝１１４）,ｒＬｓｐ．＝０．３６４,ｐ＜０．０１（ｖ＝１１４）;胫骨前肌：ｒＬｃｏｒ．＝０．３４９,ｐ＜０．０１（ｖ＝６９）,ｒＬｓｐ．＝０．３１７,ｐ＜０．０１,（ｖ＝６９）。回归方程是：鱼际：Ｌｃｏｒ．（ｍｓ）＝１２．１４８＋０．０４６Ｈ（ｃｍ）,Ｌｓｐ．（ｍｓ）＝２．０８５＋０．０６５Ｈ（ｃｍ）;胫骨前肌：Ｌｃｏｒ．（ｍｓ）＝１３．０３８＋０．０９７Ｈ（ｃｍ）,Ｌｓｐ．（ｍｓ）＝３．３９７＋０．０７８Ｈ（ｃｍ）。这样在临床工作中,只要测量出身高,就可以确定其各肌肉的皮层潜伏期、脊髓潜伏期的正常值,它将给临床工作带来方便,同时它也将给临床中枢神经疾病的诊断和预后判定提供方便。     

人体正中神经刺激的体感诱发电位观察

对30例正常成人,在 Erb 点、C_7处体表及大脑皮层相应体感区头皮(C_3或 C_4)记录正中神经刺激引起的体感诱发电位。测定了体感诱发电位各主要成分潜伏期,并计算出自腕部到 Erb 点之间正中神经外周传导速度(PCV)为70.80±2.60m/s。自 C_7到大脑皮层相应体感区之间中枢段(N_(18)-N_(13))传导时间(CCT)为5.90±0.65ms。左右两侧 PCV 和 CCT 均无显著差异(P>0.05),前者两侧之差的正常值上限为4.30m/s,后者为1.40ms。     

刺激大鼠颈體背外侧束诱发的脊髓电场电位

电刺激大鼠颈髓背外侧束(DLF),在脊髓腰段用微电极记录到—诱发场电位,将其长时程慢电位正波称为 DLF-FP。DLF-FP 的潜伏期为7.22±1.41ms,达峰时间为15.12±5.58ms,时程为93.92±9.06ms。绘制 DLF-FP 等电位图发现:其负电场中心位于背表面下1.0—1.3mm,与外周传入诱发的场电位(P_1-FP)的起源部位基本一致。印防己毒素抑制DLF-FP,士的宁加强 DLF-FP。在一定时间范围内,先后刺激腓肠神经和 DLF,两者所诱发的场电位具有总和和抑制现象。这些结果表明 DLF-FP 是初级传入末梢去极化的反映,可能和刺激外周神经诱发的场电位共用脊髓环路。     

家兔三叉神经终止核对颏舌肌肌电活动的调制作用

本工作在35只氨基甲酸乙酯麻醉、自主呼吸的家兔上观察了刺激三叉神经终止核(NTV)对颏舌肌肌电活动的影响。结果发现,电刺激NTV和NTV内微量注射谷氨酸钠都能使颏舌肌出现明显的易化效应。电刺激NTV背侧与腹侧时,颏舌肌肌电反应的潜伏期分别为5.9±0.7ms和3.0±0.4ms,电刺激舌下神经核时颏舌肌反应的潜伏期为2.2±0.2ms。结果提示三叉神经终止核的兴奋可加强颏舌肌的活动从而减小上呼吸道阻力。     

前庭—交感反应的中枢通路分析

用锋电位触发叠加(STA)技术对大鼠前庭内侧核(NVM)、下段脑干网状结构(RF)和前庭小脑进行了探查,观察了这些结构中对摆动旋转起反应的单位(PPU)与内脏大神经(SN)记录的交感反应之间的关系。发现用NVM的PPU进行STA,在SN可得一阳性反应,其潜伏期为33.28±3.1ms;用下段脑干RF的PPU进行STA,SN的峰反应潜伏期为11.3±0.91ms;用前庭小脑的PPU进行STA,SN的峰反应潜伏期为21.86±1.73ms。本结果提示前庭交感反应的最近的脊髓上中继站是下段脑干RF旁正中区核团,其下行冲动可能是由网状脊髓束中慢速传导的纤维传导的。根据三个脑区PPU引起的SN-STA潜伏期的不同,在前庭交感反应中前庭小脑所处的地位可能在NVM和下段脑干RF核团之间。     

电刺激大鼠延髓头端腹外侧区对交感节前神经元单位放电的影响

本实验用氨基甲酸乙酯麻醉和箭毒化的雄性大鼠,细胞外记录脊髓胸2节段的交感节前神经元(SPN)单位放电,电刺激同侧颈交感干,逆向激活 SPN,以确定所记录的神经元为交感节前神经元。共分析了80个 SPN 单位放电,其中有自发活动和无自发活动的单位各40个。SPN 轴突传导速度为0.59—3.75m/s。实验观察到电刺激同侧延髓头端腹外侧区(Rostralventrolateral medulla:RVL)可兴奋多数有自发活动的 SPN(19/25),并可使少数静止SPN 产生诱发反应(4/23),潜伏期为6—115ms。电刺激对侧 RVL 结果类似:多数自发活动的 SPN(6/9)呈兴奋反应,及少数静止 SPN(3/17)产生诱发反应,潜伏期为11—105ms。表明 RVL 对双侧 SPN 有兴奋性影响。     

大鼠前庭内侧核在前庭—交感反应中的作用

实验在氯醛糖和尿酯混合麻醉的大鼠上进行。在内脏大神经上记录刺激同侧前庭神经进入脑干处的交感反应。电刺激前庭神经可在同侧内脏大神经引出—明确的叠加反应,其平均潜伏期为45.8±6.98ms,时程为55.21±5.35ms。增加刺激强度,反应幅度也增加,但潜伏期不变。用前庭内侧核(NVM)的片层场电位作为指标并选择其相位倒转处作刺激点,可在同侧内脏大神经记录到潜伏期为32ms 的叠加反应,而同一动物刺激前庭神经入脑处时内脏大神经反应的潜伏期为43ms。在 NVM 头端损毁后,此前庭-交感反应明显减小,再损毁尾端 NVM 后,此反应消失。损毁 Deiters 核对前庭-交感反应无影响。这些结果表明 NVM在内脏大神经记录到的前庭-交感反应中是一重要的中继站。     

电刺激大鼠皮神经外周端对相邻脊髓节段皮神经内Aβ纤维的机械感受特性的影响

为观察Aβ类初级传入纤维是否参与相邻脊髓节段外周末梢之间的信息传递及其相关机制 ,实验自近中端切断一侧T8～T12 脊髓节段背侧皮神经 ,将一支被切断的皮神经的外周端分离成数支细束 ,以单个Aβ纤维放电为指征 ,检测单位的传导速度、适应特性、机械感受阈值、感受野的形状和面积 ;在相邻脊髓节段、也与中枢断离的皮神经干上施加逆向电刺激 ( 0 45mA ,0 1ms,2 0Hz,10s) ,以观察该刺激对Aβ纤维的上述机械感受特性的影响。在 42只大鼠上共记录了 5 0个Aβ类单位。逆向电刺激相邻节段皮神经后 ,60 6% (n =3 3 )的单位感受野增大 ,全部单位的感受野平均面积从 8 94± 6 5 1mm2 显著增加到 2 0 3 4± 16 17mm2 (P <0 0 1)。 81 8% (n =2 0 )的单位感受野形状从点状、圆或与身体长轴垂直的椭圆变成与身体长轴斜行或平行的椭圆。 68 0 % (n =5 0 )的单位机械感受阈值下降 ,全部单位的平均阈值从 2 3 7± 1 2 4mN降至 2 2 9± 1 2 4mN (P <0 0 5 )。上述机械感受特性的改变可持续 5 2 2 3± 9 2 7至 5 6 93± 15 76min。跨节段电刺激后 ,有 5 0 0 % (n =5 0 )的单位同时出现放电的增加 ,但该增加仅持续 1 5 2± 0 46min ,显著短于机械感受特性改变的时程 (P <0 0 1)。有机械感受特性改变的单位也     

高频电刺激下丘脑后核对氟哌啶醇致大鼠运动不能 的影响

目的：利用氟哌啶醇致僵直大鼠模拟帕金森病（PD）的运动不能,通过高频电刺激下丘脑后核(PH),观察大鼠僵直和运动能 力的变化,从而探讨PH 在PD治疗中潜在的应用价值。方法：将成年雄性SD 大鼠随机分为PH 刺激组、假刺激组和对照组,对 PH 刺激组和假刺激组大鼠双侧PH 置入双极刺激电极,腹腔注射氟哌啶醇30 min 后,PH刺激组给予持续高频电刺激(130 Hz,60 us, 100 uA),分别利用爬杆实验和跑步机实验评价大鼠僵直程度和运动能力。结果：腹腔注射氟哌啶醇1.0 mg/kg 后,①大鼠呈僵 直状态,其潜伏期为167.88± 17.88 s, 给予双侧PH 高频电刺激后潜伏期显著缩短至77.5± 21.27 s（P<0.01）。②跑步机试验显示大 鼠跑动速度和跑动距离显著下降,分别为5.78± 0.90 cm/s 和8.06± 4.35 m（P<0.01）,给予双侧PH高频电刺激后显著提高跑动速 度和跑动距离,分别为12.72± 3.66 cm/s 和98.61± 96.75 m（P<0.01）。结论：腹腔注射氟哌啶醇可模拟帕金森病的僵直和运动不 能症状,双侧高频电刺激PH 可显著拮抗氟哌啶醇对大鼠僵直和运动不能的作用,提示PH 为DBS治疗帕金森病运动不能的有效 刺激靶点,为临床DBS 刺激PH 治疗PD 提供实验依据。     

产后抑郁症患者听感觉门控 P50 的研究

摘要 目的： 探讨产后抑郁症患者感觉门控 P50 的变化特征,为产后抑郁患者的早期预防提供参考依据。方法： 采用配对听觉条件 (S1)、测试(S2)刺激范式, 对本院 2011 年 1 月至 2012 年 6 月收治的 26 例产后抑郁症患者(实验组)进行听觉诱发电位 P50 检测, 测量 P50 的潜伏期、 波幅, 并与 25 例健康被试者(对照组)的结果进行比较。 结果： (1) 与对照组相比, 实验组 S1-P50 潜伏期[(56.62 ± 17.42) ms vs. (49.86 ± 15.21) ms], S2-P50 潜伏期[(57.36 ± 15.42) ms vs. (50.04 ± 16.27) ms]的差异均无统计学意义(P>0.05); (2) 与对照组相比, 实验组 S1-P50 波幅[(3.58 ± 1.72) μV vs. (1.13 ± 0.91) μV]显著降低, 差异有统计学意义(P<0.05); S2-P50 波幅[ (1.32 ± 1.16) μV vs. (1.48 ± 1.05) μV]差异无统计学意义(P>0.05); (3) 与对照组相比, 实验组 S2/S1 波幅比值[(1.17 ± 0.26) vs. (0.41 ± 0.13)]显著升高, 差异有统计学意义(P<0.05)。结论： 产后抑郁症患者感觉门控抑制能力有缺陷, P50 受损指标可能为评估 产后抑郁症患者的潜在生物学指标。     

Dorsal horn administration of muscimol abolishes the muscle pressor reflex.

The purpose of this study was to determine the effect of blocking synaptic transmission in the dorsal horn on the cardiovascular responses produced by activation of muscle afferent neurons. Synaptic transmission was blocked by applying the GABA(A) agonist muscimol to the dorsal surface of the spinal cord. Cats were anesthetized with alpha-chloralose and urethane, and a laminectomy was performed. With the exception of the L(7) dorsal root, the dorsal and ventral roots from L(5) to S(2) were sectioned on one side, and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L(7) and S(1) ventral roots. The dorsal surface of the L(4)--S(3) segments of the spinal cord were enclosed within a "well" created by applying layers of vinyl polysiloxane. Administration of a 1 mM solution of muscimol (based on dose-response data) into this well abolished the reflex pressor response to contraction (change in mean arterial blood pressure before was 47 +/- 7 mmHg and after muscimol was 3 +/- 2 mmHg). Muscle stretch increased mean arterial blood pressure by 30 +/- 8 mmHg before muscimol, but after drug application stretch increased MAP by only 3 +/- 2 mmHg. Limiting muscimol to the L(7) segment attenuated the pressor responses to contraction (37 +/- 7 to 24 +/- 11 mmHg) and stretch (28 +/- 2 to 16 +/- 8 mmHg). These data suggest that the dorsal horn of the spinal cord contains an obligatory synapse for the pressor reflex. Furthermore, these data support the hypothesis that branches of primary afferent neurons, not intraspinal pathways, are responsible for the multisegmental integration of the pressor reflex.     

CL 218,872 Binding to Benzodiazepine Receptors in Rat Spinal Cord: Modulation by γ-Aminobutyric Acid and Evidence for Receptor Heterogeneity

The binding of the triazolopyridazine CL 218,872 to central benzodiazepine receptors identified with [3H]Ro 15-1788 was studied in extensively washed homogenates of rat spinal cord and cerebral cortex. CL 218,872 displacement curves were shallow in both spinal cord (nH = 0.67) and cortex (nH = 0.54), suggesting the presence of type 1 and type 2 benzodiazepine receptors in both tissues. CL 218,872 had lower affinity in spinal cord (IC50 = 825 nM) than cortex (IC50 = 152 nM), possibly reflecting the presence of fewer type 1 sites in the cord. Activating gamma-aminobutyric acid (GABA) receptors with 10 microM muscimol resulted in a two- to threefold increase in CL 218,872 affinity in both tissues without changes in the displacement curve slope. This indicates that GABA enhances CL 218,872 affinity for both type 1 and type 2 sites in both spinal cord and cerebral cortex.     

Optimal stimulation of paralyzed muscle after human spinal cord injury.

Muscle properties change profoundly as a result of disuse after spinal cord injury. To study the extent to which these changes can be reversed by electrical stimulation, tibialis anterior muscles in complete spinal cord-injured subjects were stimulated for progressively longer times (15 min, 45 min, 2 h, and 8 h/day) in 6-wk intervals. An index of muscle endurance to repetitive stimulation doubled (from 0.4 to 0.8), contraction and half-relaxation times increased markedly (from 70 to approximately 100 ms), but little or no change was measured in twitch or tetanic tension with increasing amounts of stimulation. The changes observed with 2 h/day of stimulation brought the physiological values close to those for normal (control) subjects. A decrease in the stimulation period produced a reversal of the changes. No effects were observed in the contralateral (unstimulated) muscle at any time, nor was there evidence of decreased numbers of motor units in these subjects secondary to spinal cord injury. Motor unit properties changed in parallel with those of the whole muscle. The occasional spasms occurring in these subjects are not sufficient to maintain normal muscle properties, but these properties can largely be restored by 1-2 h/day of electrical stimulation.     

Increased γ-Aminobutyric Acid Receptor Function in the Cerebral Cortex of Myoclonic Calves with an Hereditary Deficit in Glycine/Strychnine Receptors

Inherited congenital myoclonus (ICM) of Poll Hereford cattle is a neurological disease in which there are severe alterations in spinal cord glycine-mediated neurotransmission. There is a specific and marked decrease, or defect, in glycine receptors and a significant increase in neuronal (synaptosomal) glycine uptake. Here we have examined the characteristics of the cerebral gamma-aminobutyric acid (GABA) receptor complex, and demonstrate that the malfunction of the spinal cord inhibitory system is accompanied by a change in the major inhibitory system in the cerebral cortex. In synaptic membrane preparations from ICM calves, both high-and low-affinity binding sites for the GABA agonist [3H]muscimol were found (KD = 9.3 +/- 1.5 and 227 +/- 41 nM, respectively), whereas only the high-affinity site was detectable in controls (KD = 14.0 +/- 3.1 nM). The density and affinity of benzodiazepine agonist binding sites labelled by [3H]diazepam were unchanged, but there was an increase in GABA-stimulated benzodiazepine binding. The affinity for t-[3H]butylbicyclo-o-benzoate, a ligand that binds to the GABA-activated chloride channel, was significantly increased in ICM brain membranes (KD = 148 +/- 14 nM) compared with controls (KD = 245 +/- 33 nM). Muscimol-stimulated 36Cl- uptake was 12% greater in microsacs prepared from ICM calf cerebral cortex, and the uptake was more sensitive to block by the GABA antagonist picrotoxin. The results show that the characteristics of the GABA receptor complex in ICM calf cortex differ from those in cortex from unaffected calves, a difference that is particularly apparent for the low-affinity, physiologically relevant GABA receptors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ammonia Intoxication: Effects on Cerebral Cortex and Spinal Cord

The effect of an acute systemic ammonia intoxication on the metabolic states of the cerebral cortex and the spinal cord of the same animal was studied in the cat. The intravenous infusion of ammonium acetate (2 and 4 mmol/kg body weight/30 min) increased the gross levels of tissue NH4+, glutamine, glutamine/glutamate ratio, lactate, and the lactate/pyruvate ratio in the cerebral cortex and the spinal cord. Pyruvate increased, but significantly only in the spinal cord; aspartate decreased, but significantly only in the cerebral cortex. The infusion of ammonium acetate did not significantly change the levels of phosphocreatine, ATP, ADP, AMP, total adenine nucleotides, adenylate energy charge, glucose, glutamate, alpha-ketoglutarate, and malate in either tissue. The changes of NH4+, glutamine, and lactate levels as well as glutamine/glutamate and lactate/pyruvate ratios in the spinal cord correlated significantly with the corresponding changes of these metabolites in the cerebral cortex. Thus, cerebral cortex and spinal cord show certain specific and comparable metabolic changes in response to a systemic ammonia intoxication. The effect of ammonia intoxication on the increases of glutamine and lactate levels is discussed.     

Spike-triggered average torque and muscle fiber conduction velocity of low-threshold motor units following submaximal endurance contractions.

The motor unit twitch torque is modified by sustained contraction, but the association to changes in muscle fiber electrophysiological properties is not fully known. Thus twitch torque, muscle fiber conduction velocity, and action potential properties of single motor units were assessed in 11 subjects following an isometric submaximal contraction of the tibialis anterior muscle until endurance. The volunteers activated a target motor unit at the minimum discharge rate in eight 3-min-long contractions, three before and five after an isometric contraction at 40% of the maximal torque, sustained until endurance. Multichannel surface electromyogram signals and joint torque were averaged with the target motor unit potential as trigger. Discharge rate (mean +/- SE, 6.6 +/- 0.2 pulses/s) and interpulse interval variability (33.3 +/- 7.0%) were not different in the eight contractions. Peak twitch torque and recruitment threshold increased significantly (93 +/- 29 and 12 +/- 5%, P <0.05) in the contraction immediately after the endurance task with respect to the preendurance values (0.94 +/- 0.26 mN.m and 3.7 +/- 0.5% of the maximal torque), whereas time to peak of the twitch torque did not change (74.4 +/- 10.1 ms). Muscle fiber conduction velocity decreased and action potential duration increased in the contraction after the endurance (6.3 +/- 1.8 and 9.8 +/- 1.8%, respectively, P <0.05; preendurance values, 3.9 +/- 0.2 m/s and 11.1 +/- 0.8 ms), whereas the surface potential peak-to-peak amplitude did not change (27.1 +/- 3.1 microV). There was no significant correlation between the relative changes in muscle fiber conduction velocity or surface potential duration and in peak twitch torque (R2= 0.04 and 0.10, respectively). In conclusion, modifications in peak twitch torque of low-threshold motor units with sustained contraction are mainly determined by mechanisms not related to changes in action potential shape and in its propagation velocity.     

Study of the audiospinal effect on the H-reflex

Studies of the audiospinal effect on the H-reflex demonstrated that in normal test subjects and in patients with injuries to the spinal cord coupled with parapareses and in part of patients with paraplegia of the lower limbs, there was a sound-induced 30-70% increase in the amplitude of the H-reflex. As the interval between the conditioning sound and testing electric stimulations was raised, two maxima of the increment of the H-reflex amplitude within 30-40 ms and 80-100 ms were revealed. The increased H-response within these intervals seems likely to be connected with the conduction of excitation from the brain cortex via the pyramidal tract and the reticulospinal tract. Part of the patients with spinal cord injuries and paraplegia of the lower limbs did not manifest any sound-induced increase in the H-reflex. Apparently, such lack of increase is either a consequence of the functional blockade of the afferent conduction tract or that of their anatomical disturbance. The method of the audiospinal effect on the H-reflexes may be used for diagnostic purposes, namely for the determination of the conduction via the afferent cerebrospinal tract.     

Distribution of vasopressin and oxytocin in rat brain

Arginine-vasopressin and oxytocin in various portions of rat brain were determined by radioimmunoassays. The hormones were extracted from tissue samples into 0.1 N HCl and then purified partially with acetone-petroleum ether extraction. The non-equilibration method was used for the assays. In this method recovery rates of arginine-vasopressin and oxytocin were 73.0 +/- 4.4% and 75.0 +/- 3.8%, respectively. Sensitivities of the assays were 1 pg of arginine-vasopressin and 0.75 pg (0.3 microU) of oxytocin per assay tube. The higher concentrations of arginine-vasopressin and oxytocin were confirmed in the hypothalamo-neurohypophyseal system, where these hormones are synthesized, transported and stored. Relatively high concentrations of these hormones, especially oxytocin, were detected in spinal cord. Amygdala, hippocampus, limbic forebrain and pineal body contained a certain amount of arginine-vasopressin (2-20 pg/mg protein). Oxytocin (1-7 pg/mg protein) was also detected in amygdala, pons and medulla oblongata, pineal body and midbrain. The low concentrations of these hormones were also found in cerebral cortex and cerebellum.     

Changes in expiratory muscle function following spinal cord section.

Following spinal cord injury, muscles below the level of injury develop variable degrees of disuse atrophy. The present study assessed the physiological changes of the expiratory muscles in a cat model of spinal cord injury. Muscle fiber typing, cross-sectional area, muscle weight, and changes in pressure-generating capacity were assessed in five cats spinalized at the T(6) level. Airway pressure (P)-generating capacity was monitored during lower thoracic spinal cord stimulation before and 6 mo after spinalization. These parameters were also assessed in five acute animals, which served as controls. In spinalized animals, P fell from 41 +/- l to 28 +/- 3 cm H2O (means +/- SE; P < 0.001). Muscle weight of the external oblique, internal oblique, transversus abdominis, and internal intercostal muscles decreased significantly (P < 0.05 for each). Muscle weight of the external oblique, internal oblique, transversus abdominis, and internal intercostal, but not rectus abdominis (RA), correlated linearly with P (r > 0.7 for each; P < 0.05 for each). Mean muscle fiber cross-sectional area of these muscles was significantly smaller (P < 0.05 for each; except RA) and also correlated linearly with P (r > 0.55 for each; P < 0.05 for each, except RA). In spinalized animals, the expiratory muscles demonstrated a significant increase in the population of fast muscle fibers. These results indicate that, following spinalization, 1) the expiratory muscles undergo significant atrophy and fiber-type transformation and 2) the P-generating capacity of the expiratory muscles falls significantly secondary to reductions in muscle mass.