Koukkou M, Federspiel A, Bräker E, Hug C, Kleinlogel H, Merlo M C, Lehmann D
University Hospital of Clinical Psychiatry, Bern, Switzerland.
J Psychiatr Res. 2000 Jan-Feb;34(1):57-73. doi: 10.1016/s0022-3956(99)00040-0.
Based on an integrative brain model which focuses on memory-driven and EEG state-dependent information processing for the organisation of behaviour, we used the developmental changes of the awake EEG to further investigate the hypothesis that neurodevelopmental abnormalities (deviations in organisation and reorganisation of cortico-cortical connectivity during development) are involved in the pathogenesis of schizophrenia. First-episode, neuroleptic-naive schizophrenics and their matched controls and three age groups of normal adolescents were studied (total: 70 subjects). 19-channel EEG delta-theta, alpha and beta spectral band centroid frequencies during resting (baseline) and after verbal stimuli were used as measure of the level of attained complexity and momentary excitability of the neuronal network (working memory). Schizophrenics compared with all control groups showed lower delta-theta activity centroids and higher alpha and beta activity centroids. Reactivity centroids (centroid after stimulus minus centroid during resting) were used as measure of update of working memory. Schizophrenics showed partial similarities in delta-theta and beta reactivity centroids with the 11-year olds and in alpha reactivity centroids with the 13-year olds. Within the framework of our model, the results suggest multifactorially elicited imbalances in the level of excitability of neuronal networks in schizophrenia, resulting in network activation at dissociated complexity levels, partially regressed and partially prematurely developed. It is hypothesised that activation of age- and/or state-inadequate representations for coping with realities becomes manifest as productive schizophrenic symptoms. Thus, the results support some aspects of the neurodevelopmental hypothesis.
基于一个整合脑模型，该模型专注于记忆驱动和脑电图状态依赖的信息处理以组织行为，我们利用清醒脑电图的发育变化进一步研究神经发育异常（发育过程中皮质-皮质连接的组织和重组偏差）参与精神分裂症发病机制的假说。研究了首发、未使用过抗精神病药物的精神分裂症患者及其匹配的对照组，以及三个年龄组的正常青少年（共70名受试者）。静息（基线）和言语刺激后19通道脑电图的δ-θ、α和β频段质心频率被用作衡量神经网络（工作记忆）达到的复杂程度和瞬间兴奋性的指标。与所有对照组相比，精神分裂症患者表现出较低的δ-θ活动质心和较高的α和β活动质心。反应性质心（刺激后质心减去静息时质心）被用作工作记忆更新的指标。精神分裂症患者在δ-θ和β反应性质心方面与11岁儿童有部分相似之处，在α反应性质心方面与13岁儿童有部分相似之处。在我们的模型框架内，结果表明精神分裂症中神经网络兴奋性水平存在多因素引发的失衡，导致在解离的复杂程度水平上网络激活，部分退化且部分过早发育。据推测，激活与年龄和/或状态不匹配的应对现实的表征会表现为典型的精神分裂症症状。因此，结果支持了神经发育假说的某些方面。
