The relation between lorazepam-induced auditory amnesia and auditory evoked potentials.

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.