Samra S K, Bradshaw E G, Pandit S K, Papanicolaou A C, Moore B D
University of Michigan Medical Centre, Ann Arbor.
Anesth Analg. 1988 Jun;67(6):526-33.
We conducted a placebo-controlled double-blind investigation in 15 normal volunteers to study the time course of amnesia to auditory stimulation produced by lorazepam. We also studied the relationship between auditory amnesia and auditory evoked potentials to determine if long-latency auditory evoked potentials (LLAEPs) could be utilized as electrophysiologic predictors of memory. Amnesia was produced by administration of 0.05 mg/kg lorazepam intravenously. To separate the changes in LLAEPs due to generalized sedation from those associated with amnestic properties of a drug, a third group of subjects given 1.5 mg/kg secobarbital was included. Observed frequency and duration of amnesia to auditory stimulation after lorazepam was 58% and 3 hours, respectively (mean values), with marked diminuition of antirecall effect at 120 minutes. Administration of lorazepam increased the latency and decreased the amplitude of N1 and P3 components of LLAEPs. These changes appeared to be a result of generalized sedation rather than the amnestic properties of the drug. We failed to find a definite relationship between amnesia and changes in LLAEPs. We conclude that P3 component of LLAEPs cannot be utilized as an electrophysiologic predictor of amnesia in humans.
我们对15名正常志愿者进行了一项安慰剂对照双盲研究，以研究劳拉西泮产生的对听觉刺激的遗忘症的时间进程。我们还研究了听觉遗忘症与听觉诱发电位之间的关系，以确定长潜伏期听觉诱发电位（LLAEPs）是否可作为记忆的电生理预测指标。通过静脉注射0.05 mg/kg劳拉西泮产生遗忘症。为了将因全身镇静引起的LLAEPs变化与药物遗忘特性相关的变化区分开来，纳入了第三组给予1.5 mg/kg司可巴比妥的受试者。劳拉西泮后对听觉刺激的遗忘症观察到的频率和持续时间分别为58%和3小时（平均值），在120分钟时抗回忆效应明显减弱。劳拉西泮的给药增加了LLAEPs的N1和P3成分的潜伏期并降低了其振幅。这些变化似乎是全身镇静的结果而非药物的遗忘特性。我们未能发现遗忘症与LLAEPs变化之间的明确关系。我们得出结论，LLAEPs的P3成分不能作为人类遗忘症的电生理预测指标。
