van Leeuwen T H, Verbaten M N, Koelega H S, Slangen J L, van der Gugten J, Camfferman G
Department of Psychopharmacology, Faculty of Pharmacy, Rudolf Magnus Institute for Neuroscience, Utrecht University, The Netherlands.
Psychopharmacology (Berl). 1995 Dec;122(3):244-62. doi: 10.1007/BF02246546.
Eighteen males performed two vigilance tasks with static and dynamic stimuli under the influence of oxazepam (20 and 40 mg) in a placebo-controlled, double blind, crossover design. Oxazepam dose-dependently impaired overall level of performance and aggravated the decrement with time in measures of accuracy and sensitivity relative to placebo. The drug reduced the amplitudes of the P1, N1, P2N2, and P3 (dose-dependently) waves of event-related potentials (ERPs). Oxazepam aggravated the linear decline with time of the P3 amplitude only. Oxazepam impaired accuracy was related to deterioration of central processing involved in stimulus discrimination (P2N2). Impairment of response-related performance measures (RT and RI) was associated with processing manifest in the P1, N1, and P3 waves. Oxazepam effects on the amplitudes of N1 and P3 correlated with drug effects on power in alpha 1 (8-10 Hz). Drug effects on overall performance and alpha were also related; the drug effect on response speed correlated only with the drug effect on beta 1 (12.5-21 Hz). Effects of time-on-task on performance and EEG were unrelated, but oxazepam induced performance declines with time may have been caused by declines in resource allocation, as manifest in the amplitude of P3. Time effects on EEG power bands and ERP amplitudes were not significantly related to the time course of oxazepam activity. A curious dissociation emerged: both oxazepam and time-on-task impaired performance, but the drug induced a decrease of theta and alpha 1 power, whereas time-on-task increased power. Various processes play a role in performance decrements with time, and various aspects of processing may be involved in signal-detection measures which makes terms such as sensitivity quite meaningless. So-called computational processing was indistinguishable from energetic processes, which questions the validity of the distinction between these two domains. Explanations of EEG activity in terms of a unidimensional theory of arousal are untenable.
18名男性在安慰剂对照、双盲、交叉设计下,于奥沙西泮(20毫克和40毫克)影响下执行了两项分别针对静态和动态刺激的警觉任务。相对于安慰剂,奥沙西泮剂量依赖性地损害了整体表现水平,并加剧了准确性和敏感性测量指标随时间的下降幅度。该药物(剂量依赖性地)降低了事件相关电位(ERP)的P1、N1、P2N2和P3波的波幅。奥沙西泮仅加剧了P3波幅随时间的线性下降。奥沙西泮导致的准确性受损与刺激辨别(P2N2)中涉及的中枢处理功能恶化有关。与反应相关的表现指标(反应时间和反应抑制)受损与P1、N1和P3波中表现出的处理过程有关。奥沙西泮对N1和P3波幅的影响与药物对α1(8 - 10赫兹)频段功率的影响相关。药物对整体表现和α频段的影响也有关联;药物对反应速度的影响仅与药物对β1(12.5 - 21赫兹)频段的影响相关。任务持续时间对表现和脑电图的影响并无关联,但奥沙西泮导致的表现随时间下降可能是由资源分配减少引起的,如P3波幅所示。任务持续时间对脑电图频段功率和ERP波幅的影响与奥沙西泮活性的时间进程并无显著关联。出现了一种奇特的分离现象:奥沙西泮和任务持续时间均损害了表现,但药物导致θ和α1频段功率降低,而任务持续时间则使功率增加。各种过程在表现随时间下降中起作用,并且处理的各个方面可能参与信号检测测量,这使得诸如敏感性等术语变得毫无意义。所谓的计算处理与能量过程无法区分,这对这两个领域之间区分的有效性提出了质疑。基于单维唤醒理论对脑电图活动的解释是站不住脚的。