The effect of lorazepam on the motor cortical excitability in man
The effect of lorazepam on the motor cortical excitability in man
复制标题
劳拉西泮对人运动皮层兴奋性的影响
作者：
U. Ziemann;S. Lönnecker;B. Steinhoff;W. Paulus
采用局灶经颅磁刺激技术研究了短效苯二氮卓类药物劳拉西泮对11名健康志愿者运动皮质兴奋性的影响。在静息和活动的指外展肌中引起肌电反应的阈值强度、运动诱发电位的大小、皮质和外周沉默期的持续时间、配对磁刺激后皮质-皮质抑制和促进以及经胼胝体抑制被用作评估运动系统兴奋性各个方面的参数。将基线值与单次口服2.5 mg劳拉西泮后2、5和24小时获得的数据进行比较。静息和活动运动阈值以及运动诱发电位大小保持不变。皮质沉默期延长，服药后5 h效果最大，外周沉默期无延长。皮质抑制表现出更多抑制的趋势，而皮质促进作用几乎完全被抑制。经胼胝体抑制表现出不一致的抑制减少趋势。与劳拉西泮的药代动力学一样，所有的效果在2小时和5小时达到顶峰，24小时后（部分）可逆。据推测，这些发现大部分是由于劳拉西泮在运动皮质水平上增强了GABA的作用。对运动阈值和运动诱发电位大小的影响不足，可能表明这些参数在生理上不同于皮质皮质兴奋性和皮质沉默期。本文讨论了当前数据在临床癫痫学中的相关性。
The effect of the short-acting benzodiazepine lorazepam on motor cortex excitability was investigated in 11 healthy volunteers using the technique of focal transcranial magnetic stimulation. The threshold intensity for evoking an electromyographic response in the resting and active abductor digiti minimi muscle, the size of the motor evoked potential, the duration of the cortical and peripheral silent periods, the corticocortical inhibition and facilitation after paired magnetic stimuli, and the transcallosal inhibition were used as parameters to assess various aspects of motor system excitability. Baseline values were compared with data obtained 2, 5 and 24 h after a single oral dose of 2.5 mg lorazepam. Resting and active motor thresholds and the size of the motor evoked potential remained unchanged. The duration of the cortical silent period was prolonged with a maximum effect 5 h after drug intake, while the peripheral silent period did not show any lengthening at that time. The corticocortical inhibition showed a tendency toward more inhibition, while the corticocortical facilitation was almost completely suppressed. The transcallosal inhibition showed an inconsistent trend to less inhibition. In parallel to the pharmacokinetics of lorazepam, all effects peaked at 2 h and 5 h, and were (partially) reversible after 24 h. It is hypothesized that most of these findings are due to the reinforcement of GABA action by lorazepam at the level of the motor cortex. The lack of effect on motor threshold and on the size of the motor evoked potential may indicate that these parameters are physiologically distinct from corticocortical excitability and the cortical silent period. The relevance of the present data in clinical epileptology is discussed.