Fein G, Biggins C, van Dyke C
Department of Psychiatry, University of California, San Francisco.
Electroencephalogr Clin Neurophysiol. 1994 Nov;92(6):536-45. doi: 10.1016/0168-5597(94)90138-4.
Recent findings of missing or markedly attenuated P50 (or P1) auditory ERPs in Alzheimer's disease (AD) patients suggest this may be a useful diagnostic and/or prognostic marker of AD cholinergic deficits. Those studies used repetitive 1/sec clicks. Given P50's long recovery time, all but the first click in that paradigm was presented during the recovery of the P50 generation system from the response to the prior click. We studied 8 AD patients and 17 elderly controls using a paradigm incorporating 7-8 sec intervals between clicks, which allows examination of P50 generation separate from P50 recovery. With the long inter-click interval, we identified P50 responses in most AD patients and controls, and found no difference in P50 amplitude between groups. These results suggest that if there is a P50 deficit in AD patients, it is the result of the accumulative effect of repetitive stimulation, rather than a primary deficit in P50 generation.
近期研究发现,阿尔茨海默病(AD)患者存在P50(或P1)听觉事件相关电位缺失或明显减弱的情况,这表明这可能是AD胆碱能缺陷的一种有用的诊断和/或预后标志物。那些研究使用的是每秒1次的重复点击声。鉴于P50的恢复时间较长,在该模式下,除了第一次点击声外,其他所有点击声都是在P50产生系统从对前一次点击声的反应中恢复期间发出的。我们使用一种在点击声之间加入7 - 8秒间隔的模式,对8名AD患者和17名老年对照者进行了研究,这种模式能够独立于P50恢复来检测P50的产生。由于点击声之间的间隔时间较长,我们在大多数AD患者和对照者中都识别出了P50反应,并且发现两组之间P50波幅没有差异。这些结果表明,如果AD患者存在P50缺陷,那是重复刺激累积效应的结果,而不是P50产生过程中的原发性缺陷。