Nichols J M, Martin F, Kirkby K C
Department of Psychology, University of Tasmania, Hobart, Australia.
Psychopharmacology (Berl). 1993;112(4):475-82. doi: 10.1007/BF02244897.
The cognitive deficits, particularly memory impairment, observed in association with organic brain damage caused by chronic alcohol ingestion, are consistent with the profile of benzodiazepine-induced amnesia. This study examined the cognitive capabilities of a group of heavy social drinkers (n = 11) and a group of low social drinkers (n = 11) under the influence of a pharmacological challenge (lorazepam 2 mg) and a placebo treatment. Lorazepam impaired visual memory and verbal learning in both groups, but the effect of lorazepam was exacerbated in the heavy social drinkers for delayed recall of verbal material. Heavy social drinkers had lower verbal fluency scores and were less able to copy complex figures than low social drinkers whether or not the pharmacological challenge was present. Lorazepam induced deficits, in both groups, which confirmed to the classic profile of those observed in benzodiazepine-induced amnesia. The deficits, both in the absence and presence of lorazepam, shown by heavy social drinkers suggest that changes may have occurred in their brain functioning.
与长期饮酒导致的器质性脑损伤相关的认知缺陷,尤其是记忆障碍,与苯二氮䓬类药物所致失忆症的特征相符。本研究考察了一组重度社交饮酒者(n = 11)和一组轻度社交饮酒者(n = 11)在药理学激发(2毫克劳拉西泮)和安慰剂治疗影响下的认知能力。劳拉西泮损害了两组的视觉记忆和言语学习能力,但在重度社交饮酒者中,劳拉西泮对言语材料延迟回忆的影响更为严重。无论是否有药理学激发,重度社交饮酒者的言语流畅性得分均低于轻度社交饮酒者,且复制复杂图形的能力也较弱。两组中劳拉西泮诱导的缺陷均符合苯二氮䓬类药物所致失忆症的经典特征。重度社交饮酒者在有无劳拉西泮情况下均表现出缺陷,这表明他们的脑功能可能已发生变化。