MEP在吉兰--巴雷综合征患者中的应用价值

目的：探讨磁刺激运动诱发电位(MEP)在吉兰-巴雷综合征(GBS)中的诊断价值。方法：对20例GBS患者进行磁刺激MEP检测，分别刺激皮层、CV6—7、T12、L4—5、Erb点、肘部及胭窝以测定中枢及周围神经传导时间，并以20例健康正常人作对照。结果：GBS患者中枢及周围神经传导时间明显长于对照组，MEP异常率为85％。结论：GBS患者磁刺激MEP检测时中枢神经及周围神经传导时间延长，MEP阳性率高。MEP对GBS的早期诊断有重要价值。     

经颅磁刺激运动诱发电位用于癫痫的研究

经颅磁刺激运动诱发电位用于癫痫的研究李振东综述史庭慧审校经颅磁刺激（ＴＭＳ）运动诱发电位（ＭＥＰ）是一项检测运动传导通路功能的新的神经电生理技术，由Ｂａｒｋｅｒ等［１］在１９８５年首先提出。与电刺激相比，磁刺激有无痛，刺激线圈不必接触皮肤，穿过颅...     

磁、电刺激运动诱发电位的对比

磁、电刺激运动诱发电位的对比黄福南综述曹起龙审校定量检测中枢运动传导功能的运动诱发电位（ＭＥＰ）已发展成为有一定实用价值的临床神经电生理学新技术。其刺激模式有两种：电刺激和脉冲磁刺激。经历十余年的探索、研究及临床应用，证明经颅电磁刺激ＭＥＰ不仅安全、...     

脑磁运动诱发电位对脊髓、神经疾病的诊断意义

脑磁运动诱发电位是八十年代新技术。本文对32例脊髓、神经疾病进行了检测,并以40名健康人的正常均值作对照,结果提示颈椎病继发脊髓病、多发性硬化症及腓肌萎缩症的峰潜期和传导时间呈有统计意义的延迟;而脊髓空洞症则属正常范围,本法虽属初试,但对运动通路的传导功能,提供了新的检测手段。     

磁刺激运动诱发电位对S_1神经根病的诊断价值

采用磁刺激腰骶部运动神经传导时间（ＭＮＣＴ）与磁刺激窝Ｆ波相结合测定运动神经根传导时间（ＭＲＣＴ）的方法，无痛无创地评估Ｓ１神经根功能。研究对象为５０名正常受试者和３０名Ｓ１神经根受损病人。结果表明：磁刺激ＭＮＣＴ在病人组均正常，而ＭＲＣＴ却明显异常，异常率为８７％，明显高于Ｆ波潜伏期的异常率７３％。因此，磁刺激运动诱发电位（ＭＥＰ）是诊断Ｓ１神经根病的一种有很大应用价值的方法。     

重复经颅磁刺激治疗抑郁症的刺激参数的研究进展

重复经颅磁刺激是在经颅磁刺激基础上发展起来的新的神经电生理技术,它利用磁场作用于大脑皮质产生感应电流来改变皮质神经细胞的动作电位,从而影响脑内代谢和神经电活动。本文简单综述了重复经颅磁刺激治疗抑郁症的部分刺激参数。     

经颅磁刺激疗法在功能性肠病中的研究进展

功能性肠病是一种常见的胃肠道疾病综合症,其特征是在没有已知器质性病变的情况下,肠道运动和分泌功能失调,但功能性肠病的发病机制尚不明确。近年来,随着神经胃肠病学的发展,初步表明其发生和脑-肠轴关系密切。经颅磁刺激是一种非侵入性无痛性的神经系统检测和治疗技术,通过脑-肠轴能够起到调整功能性肠病的作用,为功能性肠病的治疗提供了新的方向。本文通过文献检索的方法,总结分析了近年来国内外学者使用经颅磁刺激疗法应用于肠易激综合征和功能性便秘患者的研究进展,发现经颅磁刺激疗法可以改善功能性肠病患者的肠道不适以及伴随的精神症状。     

非侵入性脑刺激对运动能力的影响

在非侵入性脑刺激(NIBS)装置中,应用广泛的是经颅磁刺激(TMS)和经颅直流电刺激(tDCS)。通过不同的TMS或tDCS刺激方案可以改变大脑皮层兴奋性,且这种兴奋性改变可长时间维持,从而具有改变突触可塑性的潜在作用。多数研究选择啮齿类动物(如大鼠和小鼠等)作为研究对象,其运动行为表现涉及运动能力、运动协调能力和运动感觉能力等。脑刺激提升运动能力的神经生物学可能机制主要体现在神经发生、神经可塑性和神经保护等方面。评估NIBS对动物模型的运动功能影响及相关的脑结构变化,将有助于探索NIBS提高脑功能的可能机制,并优化临床或实践应用的干预方案。     

前臂正中神经损害运动神经传导检测的定位诊断价值

目的探讨运动神经传导检测对前臂正中神经损害患者的定位诊断价值。方法：对56例经临床诊断的腕管综合征（CTS）、前臂外伤后正中神经损害的患者,应用常规的运动神经传导检测,检测正中神经肘-腕、腋-肘运动传导速度（MCV）;跨病变节段神经传导检测,分别在肘窝、腋窝刺激,分别将记录电极在病变部位的远端及近端记录,比较其MCV、潜伏期、波幅变化,并与患者对侧对应点的传导检测作对照。结果：①常规运动神经检测方法可以判断神经损害的大致节段;②跨病变节段神经传导检测法可以定位神经损害部位。结论：常规神经传导检测配合跨病变节段神经传导检测有较高的神经损伤定位诊断价值。     

磁刺激在脊髓损伤康复治疗中的应用进展

磁刺激在脊髓等中枢神经系统损伤疾病的康复治疗中得到了广泛应用,磁刺激作用于不同部位以及不同的治疗频率,将产生不同的治疗效果。本文综述近年来有关磁刺激治疗在脊髓损伤后运动功能障碍、神经病理性疼痛、肌张力增高、神经源性膀胱、直肠功能等方面的治疗文献,以期为临床治疗提供相关依据。     

Peripheral nerve conduction and central motor conduction after magnetic stimulation of the brain in myotonic dystrophy.

Central motor conduction time was calculated after magnetic stimulation of the brain in 15 patients with myotonic dystrophy and in 38 healthy voluntaries of the same age. Conventional electromyography and motor and sensory conduction velocities were also performed. Central motor conduction time from vertex to C8 was within the normal range in all patients whereas motor conduction velocity of the peripheral nerve and amplitude of the nerve evoked potentials were slightly reduced in 3 and 2 cases respectively, supporting peripheral nerve involvement in some subjects. Our results suggest that the reported central nervous system involvement in myotonic dystrophy, including the nonspecific white matter lesions showed by magnetic resonance imaging, would not affect the conduction of the corticospinal tracts. Magnetic stimulation on the motor cortex is a painless method to study the central nervous system and apports a satisfactory approximation to central motor pathways conduction.     

Electrophysiological characterization of the X-linked recessive bulbospinal neuronopathy (XRBSN).

Detailed electrophysiological analyses including nerve conduction velocity measurements of motor and sensory nerves, EMG recordings of a variety of muscles, evoked potentials, magnetic brain stimulation, electrophysiological testing of autonomic functions, tremor measurements and testing of voluntary movements were applied to three patients with X-linked recessive bulbospinal neuronopathy (XRBSN). All three patients presented with a slowly progressive anterior horn impairment, involvement of sensory nerves and posterior columns, but intact central descending motor pathways and an essential tremor responding to propranolol treatment. The spectrum of electrophysiological findings helps to diagnose XRBSN reliably even in sporadic cases.     

The excitability of human cortical inhibitory circuits responsible for the muscle silent period after transcranial brain stimulation

The silent period after transcranial magnetic brain stimulation mainly reflects the activity of inhibitory circuits in the human motor cortex. To assess the excitability of the cortical inhibitory mechanisms responsible for the silent period after transcranial stimulation, we studied, in 15 healthy human subjects, the recovery cycle of the silent period evoked by transcranial and mixed nerve stimulation delivered with a paired stimulation technique. The recovery cycle is defined as the time course of the changes in the size or duration of a conditioned test response when pairs of stimuli (conditioning and test) are used at different conditioning-test intervals. The recovery cycle of the duration of the silent period in the first dorsal interosseous (FDI) muscle during maximum voluntary contraction after transcranial magnetic stimulation was studied by delivering paired magnetic shocks (a conditioning shock and a test shock) at 120% motor-threshold intensity. Conditioning-test intervals ranged from 20-550 ms. The recovery cycle of the silent period in the FDI muscle during maximum voluntary contraction after nerve stimulation was evaluated by paired, supramaximum bipolar electrical stimulation of the ulnar nerve at the wrist (conditioning-test intervals ranging from 20 to 550 ms). Electromyographic activity was recorded by a pair of surface-disk electrodes over the FDI muscle. The recovery cycle of the silent period after transcranial magnetic stimulation delivered through the large round coil showed two phases of facilitation (lengthening of the silent period), one at 20-40 ms and the other at 180-350 ms conditioning-test intervals, with an interposed phase of inhibition (shortening of the silent period) at 80-160 ms. The conditioning magnetic shock left the size of the test motor-evoked potentials statistically unchanged during maximum voluntary contraction. Paired transcranial stimulation with a figure-of-eight coil increased the duration of the test silent period only at short conditioning-test intervals. Conditioning nerve stimulation left the silent period produced by test nerve stimulation unchanged. In conclusion, after a single transcranial magnetic shock, inhibitory circuits in the human motor cortex undergo distinctive short-term changes in their excitability, probably involving different mechanisms.     

The effect of transcranial magnetic stimulation on reciprocal inhibition in the human leg.

The effect of magnetic stimulation on reciprocal Ia inhibition of the human leg was investigated. Stimulation of the common peroneal nerve at the fibula head at the threshold of the alpha motoneuron axons resulted in inhibition of the soleus (SOL) H reflex at a conditioning-test interval of 2 ms. Magnetic stimulation over the contralateral motor cortex resulted in complex modulations of the SOL H reflex, including a short latency facilitation followed by inhibition. This inhibition may have been conveyed by Ia inhibitory interneurons projecting to SOL motoneurons. To test for convergence, whether or not the magnetic stimulation was capable of facilitating disynaptic reciprocal Ia inhibition of the SOL H reflex induced by stimulation of the peroneal nerve, the two stimuli were given together or separately. We observed the inhibition significantly increased when the two stimuli were given together than separately. These results suggest that the Ia inhibitory interneurons projecting to SOL motoneurons in humans might receive convergent input from the motor area of the brain and from Ia afferents of the tibialis anterior (TA) muscle in humans as well as in other animals.     

Brain temperature and exercise performance

Events arising within the central nervous system seem to be a major factor in the aetiology of hyperthermia-induced fatigue. Thus, various studies with superimposed electrical nerve stimulation or transcranial magnetic stimulation have shown that both passive and exercise-induced hyperthermia will impair voluntary motor activation during sustained maximal contractions. In humans, the brain temperature increases in parallel with that of the body core, making it very difficult to evaluate the independent effect of the cerebral temperature. Experiments with separate manipulation of the brain temperature in exercising goats indicate that excessive brain hyperthermia will directly affect motor performance. However, several homeostatic changes arise in parallel with hyperthermia, including factors that may influence both peripheral and central fatigue, and it is likely that these changes interact with the inhibitory effect of an elevated brain temperature.     

重复磁刺激右侧大脑中动脉闭塞模型大鼠脑梗死区微环境及神经功能的变化

背景：国内外大量研究表明重复经颅磁刺激可使皮质兴奋性产生较刺激时间更加持久的改变,为磁刺激应用于脑梗死后康复治疗提供了一个新的研究方向,但其远期临床疗效与安全性尚需进一步研究。 目的：观察重复经颅磁刺激脑梗死大鼠对神经再生微环境及功能恢复的影响。 方法：将大鼠随机分为模型组、假刺激组及重复经颅磁刺激组(80%运动阈值(MT)组、100%MT组和120%MT组),采用线栓法制备大鼠右侧大脑中动脉闭塞模型。制模24 h后各重复经颅磁刺激亚组给予20 Hz相应强度磁刺激,假刺激组则给予假磁刺激,模型组制模后未给予特殊处理。 结果与结论：造模后7 d,重复经颅磁刺激组的脑梗死体积显著小于模型组及假刺激组(P < 0.05)。RT-PCR、Western blot检测显示,造模后72 h,重复经颅磁刺激组水通道蛋白4/9基因和蛋白表达均较模型组显著增高(P < 0.05)。与造模后第1天比较,造模后第15天重复经颅磁刺激组(100%MT)神经功能缺损评分得到明显改善(P < 0.05)。免疫组织化学检测结果显示,各重复经颅磁刺激亚组缺血半暗带区胶质纤维酸性蛋白表达与模型组比较均显著减少(P < 0.05)。结果证实,重复经颅磁刺激可减轻脑梗死模型大鼠神经功能缺损程度,通过诱导脑缺血耐受、减少神经细胞凋亡和降低水通道蛋白4/9基因和蛋白的表达,改善神经再生微环境。中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程     

Stump nerve signals during transcranial magnetic motor cortex stimulation recorded in an amputee via longitudinal intrafascicular electrodes

Do central and peripheral motor pathways associated with an amputated limb retain at least some functions over periods of years? This problem could be addressed by evaluating the response patterns of nerve signals from peripheral motor fibers during transcranial magnetic stimulation (TMS) of corticospinal tracts. The aim of this study was to record for the first time TMS-related responses from the nerves of a left arm stump of an amputee via intrafascicular longitudinal flexible multi-electrodes (tfLIFE4) implanted for a prosthetic hand control. After tfLIFE4 implant in the stump median and ulnar nerves, TMS impulses of increasing intensity were delivered to the contralateral motor cortex while tfLIFE4 recordings were carried out. Combining TMS of increasing intensity and tfLIFE4 electrodes recordings, motor nerve activity possibly related to the missing limb motor control and selectively triggered by brain stimulation without significant electromyographic contamination was identified. These findings are entirely original and indicate that tfLIFE4 signals are clearly driven from M1 stimulation, therefore witnessing the presence in the stump nerves of viable motor signals from the CNS possibly useful for artificial prosthesis control.     

Electrical stimulation of the human common peroneal nerve elicits lasting facilitation of cortical motor-evoked potentials

Motor-evoked potentials (MEP) in the tibialis anterior (TA) muscle were shown to be facilitated by repetitive electrical stimulation of the common peroneal (CP) nerve at intensities above motor threshold. The TA electromyogram (EMG) and ankle flexion force were recorded in response to transcranial magnetic stimulation (TMS) of the leg area of the motor cortex to evaluate the excitability of cortico-spinal-muscular pathways. Repetitive stimulation of the CP nerve at 25 Hz for 30 min increased the MEP by 50.3 ± 13.6% (mean ± S.E.) at a TMS intensity that initially gave a half-maximum MEP (MEP_h). In contrast the maximum MEP (MEP_max) did not change. Ankle flexion force (103 ± 21.9%) and silent period duration (75.3 ± 12.9%) also increased. These results suggest an increase in corticospinal excitability, rather than total connectivity due to repetitive CP stimulation. Facilitation was evident after as little as 10 min of stimulation and persisted without significant decrement for at least 30 min after stimulation. The long duration of silent period following CP stimulation (99.2 ± 14.8 ms) suggests that this form of stimulation may have effects on the motor cortex. To exclude the possibility that MEP_h facilitation was primarily due to sensory fibre activation, we performed several control experiments. Preferentially activating Ia muscle afferents by vibration in the absence of motor activity had no significant effect. Cutaneous afferent activation via stimulation of the superficial peroneal nerve increased the amplitude of responses at MEP_max rather than MEP_h. Concurrent tendon vibration and superficial peroneal nerve stimulation failed to facilitate TA MEP responses. In summary, repetitive electrical stimulation of the CP nerve elicits lasting changes in corticospinal excitability, possibly as a result of co-activating motor and sensory fibres.Due to an error in the citation line, this revised PDF (published in December 2003) deviates from the printed version, and is the correct and authoritative version of the paper.     

Modulation of motor cortex excitability by median nerve and digit stimulation

We investigated the time course of changes in motor cortex excitability after median nerve and digit stimulation. Although previous studies showed periods of increased and decreased corticospinal excitability following nerve stimulation, changes in cortical excitability beyond 200 ms after peripheral nerve stimulation have not been reported. Magnetoencephalographic studies have shown an increase in the 20-Hz rolandic rhythm from 200 to 1000 ms after median nerve stimulation. We tested the hypothesis that this increase is associated with reduced motor cortex excitability. The right or left median nerve was stimulated and transcranial magnetic stimulation (TMS) was applied to left motor cortex at different conditioning-test (C-T) intervals. Motor-evoked potentials (MEPs) were recorded from the right abductor pollicis brevis (APB), first dorsal interosseous (FDI), and extensor carpi radialis (ECR) muscles. Right median nerve stimulation reduced test MEP amplitude at C-T intervals from 400 to 1000 ms for APB, at C-T intervals from 200 to 1000 ms for FDI, and at C-T intervals of 200 and 600 ms for ECR, but had no effect on FDI F-wave amplitude at a C-T interval of 200 ms. Left median nerve (ipsilateral to TMS) stimulation resulted in less inhibition than right median nerve stimulation, but test MEP amplitude was significantly reduced at a C-T interval of 200 ms for all three muscles. Digit stimulation also reduced test MEP amplitude at C-T intervals of 200–600 ms. The time course for decreased motor cortex excitability following median nerve stimulation corresponds well to rebound of the 20-Hz cortical rhythm and supports the hypothesis that this increased power represents cortical deactivation. Received: 11 December 1998 / Accepted: 30 April 1999