Bruchiel K J, Stockard J J, Calverley R K, Smith N T, Scholl M L, Mazze R I
Anesth Analg. 1978 Mar-Apr;57(2):244-51.
In 7 subjects, serial EEGs, serum bromide determinations, and psychological tests were done prior to and following 13.83 +/- 0.74 (SEM) MAC-hours of halothane anesthesia. Significant psychological impairment demonstrated 2 days following anesthesia in these subjects was absent 2 weeks following exposure to halothane. Nonspecific postanesthetic slowing of the EEG was found, qualitatively similar to but more marked than that following exposure to enflurane. Generalized EEG slowing, with a tendency toward posterior delta activity and significant reduction of frequency and amplitude of the alpha rhythm, persisted for 6 to 8 days following anesthesia. Rare sharp-wave activity developed in 3 subjects in the 1st week after halothane. A potentially psychoactive postanesthetic serum bromide level of 2.97 +/- 0.17 mEq/L (SEM) was found 5 days following anesthesia. Electroencephalographic changes characteristic of mild bromide intoxication were absent, suggesting that the psychological impairment noted after halothane anesthesia is probably not due to this metabolite; these psychological changes are probably due instead to persistence in the circulation of unchanged halothane.
对7名受试者在接受13.83±0.74（标准误）最低肺泡有效浓度-小时的氟烷麻醉前后进行了系列脑电图（EEG）检查、血清溴化物测定和心理测试。这些受试者在麻醉后2天出现了明显的心理损伤，但在接触氟烷2周后这种损伤消失了。发现麻醉后EEG出现非特异性减慢，其性质与接触恩氟烷后相似，但更为明显。广泛性EEG减慢，伴有后头部δ活动倾向以及α节律频率和波幅的显著降低，在麻醉后持续6至8天。在氟烷麻醉后的第1周，3名受试者出现了罕见的尖波活动。麻醉后5天发现血清溴化物水平为2.97±0.17 mEq/L（标准误），这一水平具有潜在的精神活性。未发现轻度溴化物中毒特征性的脑电图变化，这表明氟烷麻醉后出现的心理损伤可能并非由这种代谢产物所致；这些心理变化可能反而归因于未代谢的氟烷在循环中的持续存在。
