Graves病患者磁运动诱发电位改变的探讨

应用磁运动诱发电位(MEP)检测46例Graves(GD)病患者和50名正常对照组MEP潜伏期、波幅及中枢运动传导时间(CMCT)。GD患者MEP潜伏期延长、波幅降低及CMCT缩短,提示GD患者神经元有损害。     

感染性脱鞘性多发神经病患者膈神经根传导时间的研究

目的：初步探讨膈神经根传导时间在感染性脱鞘性多发神经病（IDP）患者的应用及特点。方法：以表面电极在肋间隙处记录20例感染性脱鞘性多发神经病患者的经项磁刺激膈神经根和经颈电刺激膈神经所得的远端运动潜伏期之差,并与31例61侧正常对照者的结果对比。结果：IDP患者较对照者膈神经根传导时间延长;膈神经根传导时间异常与临床呼吸困难相关;膈神经根传导时间的异常率高于临床呼吸困难出现率。结论：膈神经根传导时间能从电生理水平反映IDP患者与呼吸有关的脊神经根功能状态,与临床呼吸困难密切相关。膈神经根传导时间的检测有助于发现IDP患者临床下呼吸功能障碍。     

阻塞性睡眠呼吸暂停低通气综合征患者膈肌对经颅磁刺激的反应

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者经颅磁刺激(TMS)膈肌运动诱发电位(MEP)的变化及可能机制.方法 2005年6月至2006年6月就诊广州医学院第一附属医院呼吸疾病研究所的健康体检者及鼾症患者,分为健康对照组16例,单纯鼾症组7例,OSAHS轻中度组13例及重度组16例,均使用TMS结合经颈椎棘突磁刺激(CMS)及多导食管电极测定右侧膈肌MEP的潜伏期、幅值和中枢运动传导时间(CMCT),5例OSAHS患者经有效鼻持续气道正压通气(nCPAP)治疗超过2个月后复查上述指标.采用SPSS 12.0统计软件进行数据分析,检测结果 以x±s表示.结果 OSAHS重度组右侧膈肌MEP的幅值为(152±116)μV,明显低于健康对照纽的(414±201)μV、单纯性鼾症组的(352±99)μV及OSAHS轻中度组的(372±206)μV;其膈肌MEP的潜伏期和CMCT分别为(18.1±1.8)和(10.6±1.8)ms,与健康对照组的(13.9±1.6)和(7.7±1.7)ms相比,单纯性鼾症组的(14.6±1.6)和(8.1±1.6)ms以及轻中度组的(15.4±2.7)和(9.0±2.2)ms明显延长.膈肌MEP的幅值、潜伏期及CMCT与微醒觉指数、呼吸暂停最长时间、夜间最低脉搏容积血氧饱和度(SpO2)、低氧指数、SpO2<90%占总睡眠时间比例以及呼吸暂停低通气指数(AHI)均具有相关性.5例重度OSAHS患者经nCPAP治疗超过2个月后,膈肌MEP的潜伏期较治疗前缩短,分别为(17.5±0.6)和(15.5±0.7)ms.结论 OSAHS患者膈肌MEP的潜伏期和CMCT均延长,而MEP的振幅降低,这些变化可能与反复夜间低氧、二氧化碳潴留及睡眠结构紊乱有关.     

老年慢性阻塞性肺疾病患者肺功能和膈肌复合动作电位的相关性研究

目的初步探讨老年慢性阻塞性肺疾病（COPD）患者肺功能的变化与相关膈神经电生理改变的关系。方法分别对50例老年COPD患者和健康老年人进行肺功能及膈神经运动传导（PNC）、膈运动诱发电位（dMEP）及膈肌复合动作电位（dCMAP）检测。结果（1）50例老年COPD患者的呼吸功能状况显著低于非COPD健康老年人（P〈0．05）。（2）老年COPD组的PNC潜伏期平均值与健康老年人的差异无统计学意义（P〉0．05），dCMAP波幅的平均值显著低于健康老年人（P〈0．01）；老年COPD组的dMEP均正常，与健康老年人相比差异无统计学意义。（3）dCMAP波幅的降低与老年COPD患者肺功能各指标的减退相关。结论老年COPD患者肺功能的下降与dCMAP降低相关。     

低频阈上重复经颅磁刺激对脑梗死患者运动诱发电位及神经功能的影响

目的研究低频阈上重复经颅磁刺激（rTMS）对脑梗死患者运动诱发电位（MEP）及神经功能恢复的影响。方法收集大脑中动脉供血区脑梗死患者30例,随机分为刺激患侧组、刺激健侧组及自然恢复组（不接受磁刺激治疗）,每组10例。在发病后3～5d,对刺激组患者行rTMS治疗,频率为0.5Hz,70%输出强度（3.0T）,900脉冲/d,连续10d。在治疗前（试验第1天）和治疗后第10、40天记录患侧脑区运动诱发电位（MEP）的潜伏期、波幅、中枢运动传导时间（CMCT）值及美国国立卫生研究院卒中量表（NIHSS）、日常生活活动能力（ADL）评分。结果①刺激患侧组与自然恢复组、刺激健侧组及自身治疗前比较,治疗后第10和40天MEP的潜伏期缩短,波幅加大,CMCT加快,且随着治疗时间的延长,差异更显著（均P〈0.05或〈0.01）。刺激健侧组和自然恢复组比较,上述指标差异均无统计学意义（P〉0.05）;但此两组自身比较,第40天波幅和CMCT均较治疗前差异有统计学意义（P〈0.05）。②两刺激组与自然恢复组和自身治疗前比较,第10和40天NIHSS及ADL评分差异均有统计学意义,第40天差异更显著（P〈0.01）。治疗前两刺激组比较,各时间点差异均无统计学意义。③不同时间点MEP的潜伏期和CMCT均与NIHSS呈正相关,与ADL评分呈负相关;波幅与NIHSS呈负相关,与ADL评分呈正相关（P〈0.05或〈0.01）。结论rTMS作用于脑梗死患者患侧脑区,对MEP有明显影响,对神经功能恢复有促进作用;作用于健侧脑区仅对神经功能恢复有促进作用。     

不典型帕金森患者皮质脊髓束损害的电生理特点——三重刺激技术研究初探

目的 分析三重刺激技术（TST）对评价不典型帕金森患者皮质脊髓束损害的临床应用价值。方法 病例组为2009年7月在北京协和医院就诊的6例不典型帕金森患者（多系统萎缩5例，进行性核上性麻痹1例），对照组为12例年龄匹配的正常人或非神经系统疾病患者。对受试者进行右上肢小指展肌TST和传统运动诱发电位（MEP）测定，分析TST波幅比（TST测试/TST对照）、中枢运动传导时间（CMCT）、静息运动阈值（RMT）、MEP潜伏期特点。对上述电生理指标进行与病程和年龄的相关性分析。结果 与对照组相比，不典型帕金森患者的TST波幅比明显降低[（40.7%±18.6%） vs （96.8%±3.0%），P＝0.001]，RMT明显升高[（63.3±5.2） vs （48.6±8.4），P＝0.001]，MEP潜伏期和CMCT在两组间差异无统计学意义（P＞0.05）。TST和传统MEP相关参数与病程或年龄之间均未见显著性相关，但是TST波幅比与病程呈现负相关趋势。结论 TST较传统MEP能更好地评价不典型帕金森患者的皮质脊髓束损害。     

重症肌无力的膈神经和肋间神经重复电刺激

目的　探讨重症肌无力 (MG)患者膈神经重复电刺激 (PRNS)和肋间神经重复电刺激(IRNS)的特点和临床应用。方法　检测 113例MG患者PRNS、IRNS、肢体及颅神经重复电刺激 (RNS)和临床症状评分 ,并同时检测用力肺活量 (FVC)。结果　FVC取决于PRNS、IRNS及面神经RNS ;I型和Ⅱ型患者存在临床下呼吸功能障碍 ,Ⅱb型与Ⅲ型和Ⅳ型相比 ,虽PRNS波幅递减程度不同 ,但阳性率差异无显著性 ;PRNS和IRNS阳性率高于FVC和呼吸困难症状阳性率 ;PRNS敏感性高于IRNS。结论PRNS和IRNS是直接反映MG患者呼吸功能受累的神经电生理指标 ,有助于准确评估病情及进行临床分类 ;建议对Ⅱ型患者常规行PRNS和IRNS检查。     

运动诱发电位对老年人髓型颈椎病的应用价值

本文对21例老年髓型颈椎病进行了电刺激运动诱发电位(MEP)测试,结果表明,MEP异常率为90.5％。改变以中枢运动传导时间(CMCT)延迟为主,部分见双侧CMCF差值增大、皮层刺激MEP波幅降低或波形消失。MEP变化与肌力明显相关,手术后可见异常MEP改善。结果提示,MEP检查可作为检测本病患者运动功能状态的客观定量指标,对其诊断有意义。术后复查MEP,对评价手术效果及预测运动功能恢复有价值。     

经颅皮层电刺激对脑梗死病人运动功能的影响

目的 探讨经颅皮层电刺激对急性脑梗死病人运动功能恢复的疗效.方法 60例急性脑梗死病人随机分为两组,治疗组用经颅皮层电刺激加常规治疗,对照组仅用常规治疗.用Fugl-Meyer运动功能(FMA)评分法、Barthel指数评分法及经颅皮层电刺激运动诱发电位(MEP)观察病人疗效.结果 治疗30 d后, 治疗组FMA及Barthel指数得分高于对照组(P<0.01),MEP皮层电位潜伏期及CMCT均较对照组明显缩短(P<0.01),皮层电位波幅明显增高(P<0.01).结论 经颅皮层电刺激是促进急性脑梗死病人肢体运动功能恢复的有效方法.     

运动发育异常儿童听觉认知电位P300特征分析及意义

目的探讨运动发育异常儿童听觉认知电位P300特征及其临床应用价值。方法选择30例运动发育异常儿童（观察组）及30例健康儿童（对照组）,采用32导事件相关电位仪进行P300潜伏期、波幅、波形及地形图分布分析。结果与对照组比较,观察组不同脑部分区P300潜伏期延长、波幅降低、波形及地形图分布异常发生率高（P〈0.05、0.01）。结论运动发育异常儿童听觉认知电位P300特征存在典型变化,临床可将其作为此类儿童运动发育生理病理及疗效观察的参考指标。     

Ageing and central motor conduction time

The corticomotoneuronal pathway in the aged was studied using the technique of percutaneous electrical stimulation of the brain and the spinal cord. Central motor conduction time (CMCT) from the cerebral motor cortex to the cervical segment of the spinal cord (C-CMCT) was measured in 26 intact volunteers (20-85 years old) by substracting the latency to onset of EMG activity of the thenar muscle after cervical stimulation from the latency to onset of EMG activity of the same muscle after cortical stimulation. The latencies to onset of action potential of the anterior tibial muscle after cortical stimulation and the onset of action potential of the same muscle after lumbar stimulation were also measured in 11 volunteers (aged 46-67 years), and the difference between the two latencies was evaluated as the central motor conduction time from the cortex to the lumbar segment of the spinal cord (L-CMCT). Mean C-CMCT was 5.1 ms. and mean L-CMCT was 12.8 ms. Neither was related to the patient's height or age. There was no difference in either C-CMCT or L-CMCT between males and females. The results suggested that the conduction of the pyramidal tract is not affected by age, and this must be recognised when motor functions in the aged are studied.     

The central motor conductivity of genioglossus in obstructive sleep apnoea

Background and objective: During wakefulness, the electromyography (EMG) activities of upper airway dilator muscles are higher in OSA syndrome (OSAS) patients than those in normal subjects. This is believed to be related to central compensatory mechanisms. This study aimed to assess the central motor conductivity of genioglossus (GG) during wakefulness and to evaluate the compensatory site in OSAS patients. Methods: Twelve OSAS patients and 12 normal subjects were recruited to record motor evoked potential (MEP) of GG to transcranial magnetic stimulation applied at dominant‐sided anterolateral area and GG response to magnetic stimulation at the third cervical level. Stimuli were delivered at the end of expiration and inspiration respectively. The central motor conduction time (CMCT) was calculated by the latency difference between cortical and cervical stimulations. Results: The MEP latency and CMCT of GG in OSAS patients were shorter than those in normal subjects at the end of expiration (MEP latency: 6.08 ± 2.06 ms and 8.24 ± 2.66 ms, respectively, P < 0.05; CMCT: 2.41 ± 1.20 ms and 3.58 ± 1.53 ms, respectively, P < 0.05). However, only in normal subjects, GG MEP latency and CMCT showed significant decrease from the end of expiration to the end of inspiration. GG CMCT of OSAS patients at the end of expiration was closely correlated with AHI (r = ?0.797, P = 0.002), the nadir oxygen saturation (r = 0.76, P = 0.003) and the longest apnoea time (r = ?0.68, P = 0.02). Conclusions: OSAS patients have an increased central motor conductivity of GG than normal subjects. Furthermore, this increased central motor conductivity of GG is related to the severity of OSAS.     

Normal values and age-related changes in magneto-electric evoked compound muscle potentials]

A number of 57 normal subjects was investigated using transcranial magnetic stimulation of the motor cortex and transcutaneous magnetic stimulation of the spinal nerve root in order to obtain normative data for central and peripheral motor latencies. Under standardized conditions (site of stimulation, stimulus intensity, degree of voluntary tonic background activation) muscle compound action potentials were recorded from different muscles of the upper and lower extremity: M. biceps brachii, M. extensor carpi radialis, M. interosseus dorsalis I, M. vastus medialis, M. tibialis anterior, and M. extensor digitorum brevis. Onset latency, peak to peak amplitude (% of maximal M-wave), duration and configuration of the muscle compound action potentials were evaluated (Fig. 1 and Tab. 1-6). Central and peripheral motor latencies were determined by stimulation over two different points of the neuraxis (cortex/cervical or lumbar nerve roots). Central motor latencies were calculated by subtracting the peripheral conduction time from the onset latency of the fastest cortically evoked muscle response. Not only the peripheral but also the central motor latencies were found to increase in higher ages (Tab. 6). This has to be taken into account when elderly patients are examined for diagnosis of disorders of the descending motor tracts.     

Effects of Chronic and Acute Pulmonary Hyperinflation on Phrenic Nerve Conduction in Patients with COPD

Abstract

In patients with moderate-to-severe Chronic Obstructive Pulmonary Disorder (COPD), pulmonary hyperinflation can occur at rest and increase during episodes of exacerbation. Among other mechanical constraints, changes in position and configuration of the diaphragm are also induced by increased end-expiratory lung volume. Both descent and flattening of diaphragm might damage the phrenic nerves by stretching their fibers. The study aimed to investigate the phrenic nerve conduction in COPD patients in stable conditions and during COPD exacerbation. In a group of 11 COPD patients without relevant comorbidities in stable conditions and subsequently in another group of 10 COPD patients during in-hospital COPD exacerbation and recovery, measurements of functional respiratory parameters and assessment of phrenic nerves motor conduction by bilateral electric stimulation were performed concurrently. Significant increase in phrenic nerves latency (p?<?0.05), but similar amplitude of motor compound muscle action potential (cMAP) was observed in stable COPD patients vs. matched controls (p?<?0.05). However, in COPD patients with resting pulmonary hyperinflation as reliably detected by substantial Inspiratory Capacity reduction (<80% pred.), the mean bilateral latency was longer vs. COPD patients without pulmonary hyperinflation (p?<?0.02). During COPD exacerbation, in contrast with mean latency, the mean amplitude of phrenic nerves cMAP improved at discharge when compared with in-hospital admission (p?<?0.05). In stable COPD patients the velocity of phrenic nerve conduction was impaired mostly in the presence of pulmonary hyperinflation, while during COPD exacerbation where dynamic pulmonary hyperinflation abruptly occurs, the reversible decrease of cMAP amplitude does suggest a temporary, acute axonal damage of phrenic nerves, potentially contributing to diaphragmatic dysfunction in these circumstances.     

Laterality effects of human pudendal nerve stimulation on corticoanal pathways: evidence for functional asymmetry

BACKGROUND: Although motor and sensory pathways to the human external anal sphincter are bilateral, a unilateral pudendal neuropathy may still disrupt anal continence. Anal continence can, however, be preserved despite unilateral pudendal damage, and so to explain those differing observations, we postulated that pudendal innervation might be asymmetric. AIMS: To explore the individual effects of right and left pudendal nerve stimulation on the corticofugal pathways to the human external anal sphincter and thus assess evidence for functional asymmetric pelvic innervation. METHODS: In eight healthy subjects, anal sphincter electromyographic responses, evoked to transcranial magnetic stimulation of the motor cortex, were recorded 5-500 msec after digital transrectal electrical conditioning stimuli applied to each pudendal nerve. RESULTS: Right or left pudendal nerve stimulation evoked anal responses of similar latencies but asymmetric amplitudes in six subjects: dominant responses (>50% contralateral side) from the right pudendal in four subjects and from the left in two. Cortical stimulation also evoked anal responses with amplitude 448 (121) microV and latency 20.9 (1.1) msec. When cortical stimulation was preceded by pudendal nerve stimulation, the cortical responses were facilitated at interstimulus intervals of 5-20 msec. Dominant pudendal nerve stimulation induced greater facilitation of the cortically evoked responses than the non-dominant nerve. CONCLUSIONS: Cortical pathways to the external anal sphincter are facilitated by pudendal nerve conditioning, in an asymmetric manner. This functional asymmetry may explain the presence and absence of anal incontinence after unilateral pudendal nerve injury.     

Pudendus-SSEP in der Diagnostik anorektaler Funktionsstörungen

Electrophysiological examinations in differential diagnosis of anorectal functional disorders comprise electromyogram of the pelvic floor, pudendal nerve terminal motor latency (PNTML) and evaluation of cortical latency of P 40 (pudendal SSEP). Pudendal SSEP usually is done via penile stimulation, since it is technically easier to carry out than perianal stimulation. In our study we compared latencies of P 40 in penile and perianal pudendal-SSEP. We examined 40 subjects aged 34 to 72 years (mean 52.4 years) without any manifestation of a neurological, urological or proctological disease. The stimulus was administered using penile ring electrodes at the base of the penis and the penile shaft as well as a perianal surface electrode applied at right and left lateral position. Cortical latencies were evoked using the averaging method from 500 stimuli. Cortical latencies of P 40 after perianal stimulation (mean: 36.7 ms from the right, 36.9 from the left) on the average were 4.7 ms shorter than after penile stimulation (mean: 41.5 ms), a correlation to the age of the subjects was not seen. There was also only a low correlation between the latencies of penile and perianal responses within the subjects. In conclusion, our results underline the necessity of separate normal values for penile and perianal pudendal SSEP in the differential diagnosis of anorectal functional disorders. Especially when a lesion of the afferents is assumed, the evaluation of pudendal SSEP may provide valuable additional information in combination with the more common methods such as electromyogram of the anal sphincter and PNTML.     

The study of the central motor conduction time to the leg: normal findings and methodologic observations

Central motor conduction time (CMCT) is calculated by subtracting latencies from each other measured to a target muscle after transcranial brain stimulation and after stimulation of lumbar spinal nerve roots. Transcranial magnetoelectrical stimulation of the motor cortex has proved to be the most useful method. However this is not true for transcutaneous stimulation of lumbar roots. In healthy subjects electrical root stimuli given at T12/L1 produced compound muscle responses in Tibialis anterior muscles in all 18 trials. However, magnetoelectrical stimulation (100% stimulus strength) evoked responses in only 8 (Novametrix) and 12 out of 18 trials (Cadwell). Stimulation with the Digitimer D190 was less effective. Additionally compound responses after electrical root excitation were more consistent and they had a higher amplitude compared with magnetoelectrical stimulation. Regarding to these results electrical lumbar root stimulation is thought to be the advantageous method despite it is slightly more uncomfortable. Therefore normal results of CMCT to Tibialis anterior (shown in Table 1) are measured after magnetoelectrical transcranial (Digitimer D190) and transcutaneous electrical stimulation of spinal nerve roots. If the peripheral motor conduction is delayed normal values have to be adapted since CMCT is thought to involve a proximal anterior root segment. An intraspinal motor conduction time can be calculated from CMCT to upper and lower extremities.