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冷性弛缓与轴突去极化有关吗?

Is cold paresis related to axonal depolarization?

机构信息

Department of Neurology, Neuromuscular Disease Group, Rudolf Magnus Institute for Neuroscience, University Medical Center Utrecht, The Netherlands.

出版信息

J Peripher Nerv Syst. 2010 Sep;15(3):227-37. doi: 10.1111/j.1529-8027.2010.00275.x.

Abstract

Cold paresis may occur in multifocal motor neuropathy and lower motor neuron disease. It was proposed to reflect nerve lesions where axons are depolarized due to loss of Na/K-pump activity. In those circumstances, a further decrease in pump activity by cooling may induce extra depolarization, conduction block, and weakness. Evidence for this hypothesis is incomplete because it is unknown if cold induces depolarization in human motor axons and other factors may contribute to the symptoms. To solve these questions, we examined 10 normal subjects. At 37, 25, 20, and 15°C we assessed: excitability in the median nerve, decrement on 3-Hz stimulation, pulsed Doppler of a wrist artery, and thenar muscle strength. Cooling induced: (1) findings compatible with axonal depolarization on excitability testing (fanning-in of threshold electrotonus, steepened current threshold relation, increased refractory period, decreased super- and subexcitability), (2) decreased Doppler peak systolic velocity without causing ischemia, (3) decreased muscle strength and impaired muscle relaxation. Decrement tests and compound muscle action potential amplitude remained normal. The excitability findings induced by cooling were best explained by axonal depolarization due to the effect of temperature on Na/K-pump activity. The induced weakness may be explained not only by this mechanism but also by impaired muscle contraction.

摘要

冷麻痹可能发生在多灶性运动神经病和运动神经元病中。它被认为反映了轴突因钠离子/钾离子泵活性丧失而去极化的神经病变。在这种情况下,冷却进一步降低泵活性可能会导致额外去极化、传导阻滞和无力。该假说的证据并不完整,因为尚不清楚低温是否会引起人类运动轴突去极化,并且其他因素可能会导致这些症状。为了解决这些问题,我们检查了 10 名正常受试者。在 37、25、20 和 15°C 时,我们评估了:正中神经的兴奋性、3Hz 刺激时的递减、腕动脉的脉冲多普勒和鱼际肌力量。冷却引起:(1)在兴奋性测试中与轴突去极化相符的发现(阈下电紧张扩散的扇形展开、电流阈值关系变陡、不应期延长、超兴奋性和亚兴奋性降低);(2)多普勒收缩期峰值速度降低而不引起缺血;(3)肌肉力量降低和肌肉松弛受损。递减测试和复合肌肉动作电位幅度保持正常。冷却引起的兴奋性发现最好用温度对钠离子/钾离子泵活性的影响引起的轴突去极化来解释。诱导的无力不仅可以用这种机制来解释,也可以用肌肉收缩受损来解释。

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