P300 delay and attenuation in schizophrenia: Reversal by neuroleptic medication
P300 delay and attenuation in schizophrenia: Reversal by neuroleptic medication
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DOI：
10.1016/s0006-3223(97)00402-2
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发表时间：
1998-09-15
影响因子：
10.6
通讯作者：
Moore, NC
中科院分区：
文献类型：
--
作者：
Coburn, KL;Shillcutt, SD;Moore, NC
背景资料：许多研究者发现精神分裂症患者的P300波幅降低，但P300潜伏期一般都是正常的;然而文献中存在相互矛盾的结果，并且解释受到药物作用和方法学差异的混淆。本研究采用标准的听觉oddball范式比较潜伏期振幅，未使用抗精神病药的精神分裂症患者与健康对照者的P300地形图分布。然后，患者治疗6周，无论是remoxipride或氟哌啶醇，他们的P300 s进行了reassessed.Results：P300衰减和延迟之间的抗精神病药，免费的患者。没有证据表明峰侧化或振幅不对称的颞区，随后的抗精神病药物正常化P300潜伏期和增加P300振幅，但后者仍然低于正常范围内的所有，除了额区。有P300潜伏期或振幅和临床pneumatologybefore或after treatment.Conclusions之间没有相关性：发现的P300延迟精神分裂症的精神抑制药物治疗正常化以前没有报道，抗精神病药物对P300振幅和潜伏期的影响似乎是独立的临床症状的影响，不能归因于抗胆碱能活性。(C)1998年生物精神病学学会。
Background: P300 amplitude reduction in schizophrenia has been found by many investigators, but P300 latency generally has been reported to be normal; however conflicting findings are present in the literature, and interpretation has been confounded by medication effects and methodological differences.Methods: This study used a standard auditory oddball paradigm to compare the latency amplitude, and topographic distribution of P300s in neuroleptic-free schizophrenic patients with those of healthy controls. The patients then were treated for 6 weeks with either remoxipride or haloperidol, and their P300s were reassessed.Results: P300s were attenuated and delayed among neuroleptic;free patients. There was no evidence of peak lateralization or amplitude asymmetry over temporal areas, Subsequent neuroleptic medication normalized P300 latencies and increased P300 amplitudes, but the latter remained below normal limits over all except frontal areas. There were no correlations between P300 latency or amplitude and clinical symptomatology either before or after treatment.Conclusions: The finding of a P300 delay in neuroleptic-free schizophrenics that is normalized by neuroleptic medication has not been reported previously, Neuroleptic effects on P300 amplitude and latency appear to be independent of effects on clinical symptoms, and cannot be attributed to anticholinergic activity. (C) 1998 Society of Biological Psychiatry.