Rippon Gina, Brock Jon, Brown Caroline, Boucher Jill
School of Life and Health Sciences (Psychology), Aston University, UK.
Int J Psychophysiol. 2007 Feb;63(2):164-72. doi: 10.1016/j.ijpsycho.2006.03.012. Epub 2006 Jul 3.
In 2002, we published a paper [Brock, J., Brown, C., Boucher, J., Rippon, G., 2002. The temporal binding deficit hypothesis of autism. Development and Psychopathology 142, 209-224] highlighting the parallels between the psychological model of 'central coherence' in information processing [Frith, U., 1989. Autism: Explaining the Enigma. Blackwell, Oxford] and the neuroscience model of neural integration or 'temporal binding'. We proposed that autism is associated with abnormalities of information integration that is caused by a reduction in the connectivity between specialised local neural networks in the brain and possible overconnectivity within the isolated individual neural assemblies. The current paper updates this model, providing a summary of theoretical and empirical advances in research implicating disordered connectivity in autism. This is in the context of changes in the approach to the core psychological deficits in autism, of greater emphasis on 'interactive specialisation' and the resultant stress on early and/or low-level deficits and their cascading effects on the developing brain [Johnson, M.H., Halit, H., Grice, S.J., Karmiloff-Smith, A., 2002. Neuroimaging of typical and atypical development: a perspective from multiple levels of analysis. Development and Psychopathology 14, 521-536]. We also highlight recent developments in the measurement and modelling of connectivity, particularly in the emerging ability to track the temporal dynamics of the brain using electroencephalography (EEG) and magnetoencephalography (MEG) and to investigate the signal characteristics of this activity. This advance could be particularly pertinent in testing an emerging model of effective connectivity based on the balance between excitatory and inhibitory cortical activity [Rubenstein, J.L., Merzenich M.M., 2003. Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior 2, 255-267; Brown, C., Gruber, T., Rippon, G., Brock, J., Boucher, J., 2005. Gamma abnormalities during perception of illusory figures in autism. Cortex 41, 364-376]. Finally, we note that the consequence of this convergence of research developments not only enables a greater understanding of autism but also has implications for prevention and remediation.
2002年,我们发表了一篇论文[布罗克,J.,布朗,C.,布彻,J.,里彭,G.,2002年。自闭症的时间绑定缺陷假说。《发展与心理病理学》142,209 - 224],强调了信息处理中“中央连贯性”心理模型[弗里思,U.,1989年。《自闭症:解开谜团》。布莱克韦尔,牛津]与神经整合或“时间绑定”神经科学模型之间的相似之处。我们提出,自闭症与信息整合异常有关,这种异常是由大脑中专门的局部神经网络之间的连接性降低以及孤立的单个神经集合内可能的过度连接所导致的。本文更新了这一模型,总结了研究中的理论和实证进展,这些进展表明自闭症存在连接紊乱。这是在自闭症核心心理缺陷研究方法发生变化的背景下进行的,这种变化更加强调“交互特化”,以及由此对早期和/或低水平缺陷及其对发育中大脑的级联效应的重视[约翰逊,M.H.,哈利特,H.,格赖斯,S.J.,卡米洛夫 - 史密斯,A.,2002年。典型与非典型发育的神经影像学:多层次分析的视角。《发展与心理病理学》14,521 - 536]。我们还强调了连接性测量和建模方面的最新进展,特别是利用脑电图(EEG)和脑磁图(MEG)追踪大脑时间动态以及研究这种活动的信号特征的新能力。这一进展在测试基于兴奋性和抑制性皮层活动平衡的有效连接性新兴模型时可能特别相关[鲁宾斯坦,J.L.,梅泽尼奇,M.M.,2003年。自闭症模型:关键神经系统中兴奋/抑制比例增加。《基因、大脑与行为》2,255 - 267;布朗,C.,格鲁伯,T.,里彭,G.,布罗克,J.,布彻,J.,2005年。自闭症患者在感知虚幻图形时的伽马异常。《皮层》41,364 - 376]。最后,我们指出,这些研究进展的融合不仅有助于更深入地理解自闭症,而且对预防和治疗也具有重要意义。