Estrin W J, Moore P, Letz R, Wasch H H
Department of Neurology, University of California, San Francisco.
Clin Pharmacol Ther. 1988 Jan;43(1):86-90. doi: 10.1038/clpt.1988.15.
Without the availability of objective measures of central neurologic dysfunction, neuroepidemiologic investigations of individuals exposed to psychoactive drugs and potential environmental and occupational neurotoxins are extraordinarily difficult, particularly when the central nervous system manifestations are subtle, diffuse, and limited to cognitive deficits. In an attempt to assess and quantitate psychomotor dysfunction, P-300 event-related potentials, Symbol Digit Test, Continuous Performance Test, and Finger Tapping Test were obtained from six subjects sequentially exposed to nitrous oxide at 0%, 10%, 20%, and 40%. With increasing concentration of N2O, there was prolongation of P-300 latency and worsening of Continuous Performance Test and Symbol Digit Test performance; P-300 amplitude and Finger Tapping Test performance were decreased by exposure to N2O. This study demonstrates a dose-dependent reduction in P-300 amplitude and prolongation of P-300 latency in subjects in whom psychomotor impairment was induced by the acute administration of N2O.
由于缺乏中枢神经功能障碍的客观测量方法，对接触精神活性药物以及潜在环境和职业神经毒素的个体进行神经流行病学调查极为困难，尤其是当中枢神经系统表现细微、弥漫且仅限于认知缺陷时。为了评估和量化精神运动功能障碍，对6名受试者依次给予0%、10%、20%和40%的氧化亚氮，并记录其P-300事件相关电位、符号数字试验、连续操作试验和手指敲击试验结果。随着氧化亚氮浓度的增加，P-300潜伏期延长，连续操作试验和符号数字试验表现恶化；暴露于氧化亚氮会使P-300波幅和手指敲击试验表现降低。本研究表明，急性给予氧化亚氮导致精神运动功能损害的受试者中，P-300波幅呈剂量依赖性降低，P-300潜伏期延长。
