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实验性局灶性压迫对人正中运动轴突兴奋性的影响。

Effects of experimental focal compression on excitability of human median motor axons.

作者信息

Ikemoto Tatsunori, Tani Toshikazu, Taniguchi Shinichirou, Ikeuchi Masahiko, Kimura Jun

机构信息

Department of Orthopaedic Surgery, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.

出版信息

Clin Neurophysiol. 2009 Feb;120(2):342-7. doi: 10.1016/j.clinph.2008.09.082. Epub 2008 Dec 19.

Abstract

OBJECTIVE

To characterize the effect of focal compression by threshold tracking and other excitability measures of human median motor axons.

METHODS

We conducted a sequence of excitability studies using a software written in BASIC (QTRAC version 4.0, (c)Institute of Neurology, London, UK, with multiple excitability protocol TRONDXM 2) in 24 healthy subjects, stimulating the median nerve at the wrist and recording compound muscle action potentials from the abductor pollicis brevis. Constant, localized compression was applied at the wrist by mechanically lowering a probe attached to a disk electrode, which also served as the stimulating cathode.

RESULTS

Compared with the pre-compression values, measurements during compression showed a shift of threshold electrotonus waveforms toward the baseline (fanning-in), steeper current-threshold relationships, increased strength-duration time constants, prolonged relative refractory periods and reduced levels of superexcitability, but no alteration in late subexcitability. These excitability changes indicating depolarization reversed to hyperpolarization immediately after release of compression. The nerve compression altered none of the excitability measures when recorded 2 cm distally from the pressure probe.

CONCLUSIONS

Mild nerve compression produces a very localized axonal depolarization at the compression site followed by hyperpolarization upon release of compression, as expected from focal ischemia.

SIGNIFICANCE

The current results imply that the sharply-localized conduction abnormalities demonstrated electrophysiologically in peripheral nerve entrapment syndromes and compression myelopathies may, in part, result from compression-induced focal nerve ischemia.

摘要

目的

通过阈值跟踪及其他人体正中运动轴突兴奋性测量方法来描述局灶性压迫的影响。

方法

我们使用用BASIC编写的软件(QTRAC版本4.0,(c)英国伦敦神经病学研究所,采用多兴奋性方案TRONDXM 2)对24名健康受试者进行了一系列兴奋性研究,刺激腕部正中神经并记录拇短展肌的复合肌肉动作电位。通过机械降低连接到盘状电极的探头(该探头也用作刺激阴极)在腕部施加恒定的局部压迫。

结果

与压迫前的值相比,压迫期间的测量显示阈下电紧张电位波形向基线偏移(扇形内聚)、电流-阈值关系更陡峭、强度-时间常数增加、相对不应期延长以及超兴奋性水平降低,但晚期亚兴奋性无变化。这些表明去极化的兴奋性变化在压迫解除后立即逆转至超极化。当在距压力探头远端2 cm处记录时,神经压迫未改变任何兴奋性测量指标。

结论

轻度神经压迫在压迫部位产生非常局部的轴突去极化,随后在压迫解除时发生超极化,这与局灶性缺血预期的情况一致。

意义

目前的结果表明,在周围神经卡压综合征和压迫性脊髓病中电生理显示的尖锐局部传导异常可能部分是由压迫引起的局灶性神经缺血所致。

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