Freigang B, Kevanishvili Z S
Arch Otorhinolaryngol. 1975 Nov 30;211(2):81-92. doi: 10.1007/BF01221116.
The investigators carried out threshold determinations on 16 children and 6 adults in wakefulness, under general anaesthesia (we used chloral hydrate anaesthesia) and in sleep (stage II-III and stage REM). Falling asleep (stage I and initial stage of anaesthesia respectively) the latencies of the individual components of the acoustically evoked potentials are prolonged in mean of 30 msec. Simultaneously the amplitude of N1 significantly decreases and N2 becomes a prominent point (Fig. 1). The generation mechanisms of wave N2 are obviously different from those of wave N1. Its input-output curve takes a very steep course (Fig. 5) and the shortening of latencies increases with growing intensity of stimulus too (Fig. 4). Amplitude histogrammes demonstrated the dependency of the form of the acoustically evoked potential on the degree of synchronisation of EEG activity. While in the case of desynchronisation N1 appears more markedly, N2 does in the case of synchronisation. The mean deviation of the ERA threshold totals plus 3.8 +/- 6.9 dB (n = 41) under chloral hydrate anaesthesia, plus 4.9 +/- 6.7 dB (n = 37) in natural sleep in contrast to the wakefulness. With a 99% confidence there occur confidence intervals ranging from + 1 to + 7 dB and from +2 to +8 dB respectively. In identifying the threshold potentials error I (existing potential not recognized) occurred in 15-20%, error II (random wave seen as potential) in 20% of these studies. All these experiments showed significant lower variances for the latencies compared with variancies of amplitudes. The variance of amplitudes is smallest in children (Table 1) under general anaesthesia as well as in adults in wakefulness (Table 2). For the practical performance of ERA chloral hydrate is recommended for studies on children. A uniform EEG-state as well as a uniform depth of sleep are basic conditions for ERA during sleep, sedation or under anaesthesia. These conditions must constantly be controlled by EEG, EOG and EMG.
研究人员对16名儿童和6名成人在清醒、全身麻醉(我们使用水合氯醛麻醉)和睡眠(II-III期和快速眼动期)状态下进行了阈值测定。入睡时(分别为I期和麻醉初期),听觉诱发电位各成分的潜伏期平均延长30毫秒。同时,N1波幅显著降低,N2波成为突出点(图1)。N2波的产生机制明显不同于N1波。其输入-输出曲线呈非常陡峭的走势(图5),潜伏期的缩短也随着刺激强度的增加而增加(图4)。振幅直方图显示听觉诱发电位的形态依赖于脑电图活动的同步程度。在去同步化时N1波更明显,而在同步化时N2波更明显。与清醒状态相比,水合氯醛麻醉下ERA阈值的平均偏差总计为+3.8±6.9dB(n=41),自然睡眠时为+4.9±6.7dB(n=37)。在99%的置信度下,置信区间分别为+1至+7dB和+2至+8dB。在这些研究中,识别阈值电位时,I类错误(存在的电位未被识别)发生率为15%-20%,II类错误(将随机波视为电位)发生率为20%。所有这些实验表明,与波幅的方差相比,潜伏期的方差显著更低。在全身麻醉下儿童的波幅方差最小(表1),在清醒状态下成人的波幅方差最小(表2)。对于ERA的实际操作,推荐使用水合氯醛进行儿童研究。在睡眠、镇静或麻醉期间,均匀的脑电图状态以及均匀的睡眠深度是ERA的基本条件。这些条件必须通过脑电图、眼电图和肌电图不断进行监测。