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自主过度通气诱发的感觉异常和手足搐搦。人类皮肤和运动轴突兴奋性增加。

Paraesthesiae and tetany induced by voluntary hyperventilation. Increased excitability of human cutaneous and motor axons.

作者信息

Macefield G, Burke D

机构信息

Department of Clinical Neurophysiology, Prince Henry Hospital, Sydney, NSW, Australia.

出版信息

Brain. 1991 Feb;114 ( Pt 1B):527-40. doi: 10.1093/brain/114.1.527.

Abstract

Anxiety can induce hyperventilation, and the resultant hypocapnia and hypocalcaemia can lead to paraesthesiae and tetany. To define the nature of the disturbance created in peripheral nerve, the excitability of cutaneous and motor axons was monitored in 6 normal subjects requested to hyperventilate until paraesthesiae developed in the hands, face and trunk. This occurred when alveolar PCO2 (PACO2) had declined on average by 20 mmHg. Spontaneous EMG activity developed when PACO2 had declined by a further 4 mmHg. Changes in the excitability of cutaneous and motor axons were measured from changes in the compound action potentials evoked by stimulation of the median nerve at the wrist and recorded over the digital nerves of the index finger and over the thenar muscles, respectively. As PACO2 declined, the size of the compound sensory and muscle potentials evoked by a constant stimulus progressively increased, indicating an increase in axonal excitability. These changes occurred before paraesthesiae or tetany developed. In each subject there was a statistically significant inverse correlation between PACO2 and axonal excitability. Independent of this increase in axonal excitability, there was no significant change in the supernormal phase of the recovery cycle of cutaneous axons. Microneurographic recordings from the median nerve in 2 subjects revealed spontaneous bursting activity of cutaneous axons, perceived as paraesthesiae. It is concluded that the paraesthesiae and tetany induced by hyperventilation result solely from changes in the excitability of cutaneous and motor axons in the peripheral nerve, presumably due to an alteration in the electrical properties of the axonal membrane resulting from a reduced plasma [Ca2+]. The supernormal phase may entrain the ectopic discharge and thereby determine the maximal discharge frequency of impulses in ectopically generated trains, but does not otherwise contribute to the physiological disturbance.

摘要

焦虑可诱发过度通气,由此产生的低碳酸血症和低钙血症可导致感觉异常和手足搐搦。为明确外周神经所产生紊乱的性质,对6名正常受试者进行监测,要求他们过度通气直至手部、面部和躯干出现感觉异常。当肺泡PCO₂(PACO₂)平均下降20 mmHg时出现这种情况。当PACO₂再下降4 mmHg时,自发肌电图活动出现。通过刺激腕部正中神经诱发复合动作电位,并分别在示指指神经和大鱼际肌上记录,根据复合动作电位的变化来测量皮肤和运动轴突兴奋性的改变。随着PACO₂下降,恒定刺激诱发的复合感觉和肌肉电位的大小逐渐增加,表明轴突兴奋性增加。这些变化在感觉异常或手足搐搦出现之前就已发生。在每个受试者中,PACO₂与轴突兴奋性之间存在统计学上显著的负相关。与轴突兴奋性的这种增加无关,皮肤轴突恢复周期的超常期没有显著变化。对两名受试者正中神经的微神经图记录显示皮肤轴突有自发爆发活动,被感知为感觉异常。得出的结论是,过度通气诱发的感觉异常和手足搐搦完全是由于外周神经中皮肤和运动轴突兴奋性的变化所致,推测是由于血浆[Ca²⁺]降低导致轴突膜电特性改变。超常期可能会引发异位放电,从而决定异位产生的冲动序列中的最大放电频率,但在其他方面对生理紊乱没有影响。

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