自闭症碎镜理论之迷思:缘起、问题与前景

自闭症患者在社会沟通和交往障碍上主要涉及社会情感互动缺陷、非语言行为交流缺陷、发展维持和理解人际关系的缺陷。该群体在社会认知过程中潜在自动的直觉成分受损被视为其独特的临床症状。鉴于镜像神经元系统在社会认知的直觉成分上扮演的重要角色,该系统的功能障碍假说(或称"碎镜"理论)被提出并用以解释自闭症的成因及其异常表现。然而,在经历了10年的发展与证据检验后,该理论潜在的问题逐渐暴露。当前的研究显示,迄今为止人类镜像神经元系统的研究存在内在缺陷,镜像神经元系统至多是社会认知的附带原因,该系统功能障碍也并非自闭症患者社会认知障碍的必要条件。碎镜理论面临来自临床行为研究与认知神经科学实验证据的广泛质疑。未来,伴随自闭症研究对象的变化,镜像神经元的社会响应学说的提出,双个体范式、第二人称神经科学范式与计算精神病学的兴起,镜像神经元与自闭症的真正关系将有望得以阐明。     

镜像神经元系统的研究回顾及展望

镜像神经元系统的发现使得研究者从一个较为统一的神经机制层面了解人类多个层次的社会认知活动。在猕猴大脑F5区发现的镜像神经元可以在抽象的层面上帮助猕猴理解他人行为的意图。利用脑成像技术,研究发现人类的镜像神经元系统能够匹配外界的知觉表征和内在的动作表征从而通过“居身模仿”这一过程来进行模仿、语言理解、理解他人的意图及情绪这些重要的社会认知活动。另外,镜像神经元系统在社会交往中也起着重要作用,最后,就镜像神经元系统在心理理论中的作用、了解自我-他人问题和镜像神经元系统的关系、动机、经验等因素对镜像神经元系统活动的调控等问题对未来的研究方向进行了展望     

镜像神经元是认知科学的“圣杯”吗?

镜像神经元作为近二十年来神经科学领域内最重要的发现之一,相关的一系列研究掀起了一场"理解社会行为的革命"。然而,通过系统考察镜像神经元最初的操作性定义、基本功能及其实验证据,发现许多研究者对于镜像神经元的定义存在误解,人类脑中是否存在镜像神经元及其功能依然是当前学术界的争议焦点。迄今仍然缺乏令人信服的证据表明镜像神经元(或系统)就是动作理解、动作模仿、共情以及读心的直接神经机制。因此,将镜像神经元视为"认知科学的圣杯"的主张是一种落后的模块论意识形态,只能催生新的"神经神话"。     

模仿心理机制研究的历史、现状与展望

近年来模仿机制研究在深化皮亚杰理论的基础上,深入探讨了模仿与心理理解之间的发生、发展关系及其相互作用机制,并结合脑神经科学研究的最新进展,探讨模仿背后的脑神经机制。在梳理当前心理学、脑神经科学中TT理论、ST理论以及镜像神经理论研究的基础上,给出了进一步深化研究的展望。     

自闭症谱系儿童模仿缺陷的脑神经机制

模仿在人类生命进化中具有举足轻莺的意义,自闭症儿童的认知发展的研究表明,模仿缺陷是导致自闭症谱系儿童沟通障碍、社交困难的核心缺陷.而镜像神经系统机能失常假设有力地解释了自闭症谱系儿童模仿缺陷的神经机制.尽管镜像神经系统的信息加工过程还存在着MOSAIC模型和EP-M模型的争论.但这两种模型都支持自闭症儿童脑神经功能连通异常的假说.     

镜像神经元的意义

镜像神经元是一种感觉–运动神经元。它的典型特征是在动作观察和动作执行两个阶段皆被激活。多年来, 由于研究伦理的限制, 研究恒河猴时使用的单细胞电极植入方式无法应用于人类, 因而不能确定人类大脑皮层是否也存在着具有同样功能的神经细胞。但是通过脑成像技术, 神经科学家确定人类大脑皮层存在着具有相同或类似功能的脑区, 称为“镜像神经系统”。文章对镜像神经元及其人类镜像神经系统的意义进行了深入分析, 指出：(1)由于镜像机制把动作知觉和动作执行进行匹配, 观察者仅仅通过他人行为的知觉, 就激活了执行这一动作的神经环路, 产生了一种他人动作的具身模拟, 因而可以直接把握他人的行为意图; (2)镜像神经元所表现出来的那种动作知觉与动作执行的双重激活功能支持了身心一体说, 从方法论上证明了身心二元论的缺陷, 为身心的整体观提供了神经生物学的证据; (3)镜像神经机制把他人的动作与自己的运动系统相匹配, 以自身动作的神经环路对他人的动作做出回应, 促进了人际理解和沟通, 成为社会沟通的“神经桥梁”。     

孤独症与镜像神经元

孤独症是起始于婴幼儿时期的由脑功能障碍引起的长期发展性障碍,有3种典型的症状:社会交往与言语沟通障碍及出现刻板僵化行为.孤独症的病因复杂,镜像神经元的发现和研究,使得研究者有望揭开孤独症症状背后的神经机制,并为孤独症的诊断和治疗予以新的启发.     

孤独症儿童动作发展障碍的神经机制

动作发展障碍(Developmental motor disorders)是孤独症谱系障碍的常见特征。通过系统回顾孤独症儿童动作发展障碍的神经科学研究, 发现γ-氨基丁酸和5-羟色胺浓度的改变及γ-氨基丁酸相关蛋白和Shank蛋白的表达异常不仅会损害中枢神经系统的发育, 而且还能导致突触兴奋性与抑制性失衡, 进而改变孤独症儿童小脑和大脑皮层运动区的功能连接。孤独症儿童小脑、基底神经节和胼胝体结构的改变对全脑的连通性产生了负面影响。神经生化机制和脑结构的异常共同导致了脑功能的异常, 最终造成孤独症儿童的动作发展障碍。此外, 动作发展障碍与孤独症核心症状共同的神经基础主要包括镜像神经元系统紊乱, 丘脑、基底神经节和小脑异常以及SLC7A5和PTEN 基因突变。未来研究需要关注与运动密切相关的其他神经递质, 如乙酰胆碱和多巴胺; 探索动作发展障碍神经网络的动态机制及其形成; 剖析该障碍的神经机制和自闭症核心症状神经机制的相互作用。     

情绪具身观：情绪研究的新视角

情绪具身性有着广泛的理论假说与研究证据, 从情绪外周理论到面部反馈假说、躯体标记假说再到现在的情绪具身观, 都一致认为情绪是具身的。情绪具身观认为情绪是包括大脑在内的身体的情绪, 身体的解剖学结构、身体的活动方式、身体的感觉和运动体验决定了我们怎样加工情绪。相关的行为和脑机制研究均支持了情绪加工的具身性。目前关于具身情绪的理论解释主要有镜像神经元系统假说、具身模仿论和知觉符号系统理论等。作为一种新兴的理论观点, 情绪具身观为情绪研究提供了新的视角。     

μ波抑制的界定、功能及其应用——揭示镜像神经元活动的机制和意义

近年来人们十分热衷对镜像神经元系统的研究,最新研究趋势是探究μ节律与镜像神经元系统活动功能的关联,文章从四个方面阐述了μ波抑制是代表高级神经活动标记的重要指标。文章首先介绍了μ波抑制机理,强调了μ波抑制功能概念的飞跃,综述了μ波抑制在三个方面(动作、语言认知、以及高级社会功能)作为镜像神经元活动的证据,最后总结与展望μ波抑制对心理与行为困难的矫正的应用。     

自闭症儿童依恋研究述评

摘要　　研究者曾一度认为自闭症儿童无法建立起依恋关系。本文系统回顾了自闭症儿童依恋研究的最新进展,将自闭症儿童是否存在依恋行为（尤其是安全型依恋行为）、依恋发展解释理论、研究方法、类型分布以及影响因素等问题进行了详细梳理,并结合研究分析,提出有关自闭症儿童依恋研究的几点启示,以供参考。     

Evaluating the Theory-of-Mind Hypothesis of Autism

ABSTRACT— Two decades ago, the theory-of-mind hypothesis of autism was introduced by Baron-Cohen and his colleagues; this theory provided a unified cognitive explanation for the key social and communication symptoms in that disorder. I evaluate the theory-of-mind hypothesis in light of studies that have addressed several key questions: Do children with autism develop theory-of-mind concepts? How can we explain why some children with autism pass theory-of-mind tasks? Do deficits in theory of mind account for the major impairments that characterize autistic disorder? Current research supports the view that autism involves delays and deficits not only in the development of a theory of mind but also in additional aspects of social-affective information processing that extend beyond the traditional boundaries of theory of mind.     

Minding the gap between neuroscientific and psychoanalytic understanding of autism

This paper offers an integrative approach to the increasingly complex puzzle of autistic spectrum disorders. The author demonstrates how the work of one group of neuroscientists in Parma, on a special class of brain cells called ‘mirror neurons', and the work of researchers at the University of California in San Diego, applying these findings to the problem of autism, intersect with Frances Tustin's discoveries about the nature, function and meaning of psychogenic autism in children and even autistic states in neurotic adults. Included in the author's considerations are the results of some by now well-known studies conducted by a group of biologists at the University of California at Berkeley in the 1960s on the effects of ‘enriched’ versus ‘deprived’ environments upon the development of the brain, and a study of autistic children diagnosed as brain damaged and treated psychoanalytically at the Paediatric Neuro-Psychiatric Institute of the University of Rome in the 1980s. The author concludes with a coherent picture of various dimensions of autistic phenomenon that may constitute more than just the sum of its parts, and points towards new areas for discussion and study.     

Unbroken mirrors: challenging a theory of Autism

The 'broken mirror' theory of autism has received considerable attention far beyond the scientific community. This theory proposes that the varied social-cognitive difficulties characteristic of autism could be explained by dysfunction of the mirror neuron system, thought to play a role in imitation. We examine this theory and argue that explaining typical imitation behavior, and the failure to imitate in autism, requires much more than the mirror neuron system. Furthermore, evidence for the role of the mirror neuron system in autism is weak. We suggest the broken mirror theory of autism is premature and that better cognitive models of social behavior within and beyond the mirror neuron system are required to understand the causes of poor social interaction in autism.     

A transactional systems model of autism services

There has been an escalation in the number of children identified with autism spectrum disorders in recent years. To increase the likelihood that treatments for these children are effective, interventions should be derived from sound theory and research evidence. Absent this supportive foundation, intervention programs could be inconsequential if not harmful. Although atypical, the development of children with autism should be considered initially from the perspective of the same variables that affect the development of typical children. In addition, the developmental deviations that characterize autism must be considered when developing intervention programs. Behavioral systems models describe both typical and atypical development and emphasize dynamic multidirectional person-environment transactions. The environment is viewed as having multiple levels, from the individuals with autism themselves, to larger societal and cultural levels. Behavioral systems models of human development can be generalized to a transactional systems model of services for children with autism. This model is the foundational theoretical position of the Southern Illinois University Center for Autism Spectrum Disorders. The center's programs are described to illustrate the application of the model to multiple levels of the social ecology.     

西方关于自闭症研究的新进展——与心理理论的关系研究

自闭症是一种罕见的身体机能失调的综合病症。本文阐述了西方关于自闭症研究的新进展,其中分别介绍了自闭症的重要症状、自闭症起因的理论假设以及自闭症与心理理论的关系研究。在阐述的过程中强调了心理理论的缺失是自闭症产生的重要原因。     

高功能自闭症个体对威胁性情绪面孔的注意偏向

高功能自闭症(High-Functioning Autism, HFA)个体智力正常, 但也面临着严重的社会功能障碍。对威胁性情绪面孔的注意偏向与HFA个体社会功能的发展密切相关。梳理相关研究发现, HFA个体在自动加工阶段和情绪目标参与阶段, 不存在威胁性情绪面孔注意偏向; 而在任务与情绪无关的控制加工阶段, 存在威胁性情绪面孔注意偏向。针对HFA个体威胁性情绪面孔注意偏向的理论解释主要有杏仁核理论、强烈世界理论和执行功能理论等。神经生理机制方面, HFA个体对威胁性情绪面孔的注意偏向可能与其异常的皮下及皮层通路功能有关, 同时可能会受5-羟色胺系统基因及催产素水平等的影响。未来研究可在综合考虑研究方法及个体因素的基础上, 进一步探究其加工特征及神经生物机制, 着力开发科学有效的干预策略。     

The neurocognitive basis of autism

The cognitive study of the underlying mental abnormalities in autism has advanced rapidly, while the biological study of the underlying brain abnormalities and of putative genetic mechanisms is lagging somewhat behind. However, the linking of cognitive and biological studies has become a real possibility. Developmental cognitive neuroscience has transformed our understanding of this enigmatic disorder, which was once misguidedly thought to be caused by maternal rejection. The hypothesis of a specific theory of mind deficit was a crucial step in this process. It explains the puzzle of the characteristic social and communication impairments of autism and allows for the fact that they can coexist with good general abilities. This hypothesis has been widely accepted and a start has been made at pinpointing the brain basis of theory of mind. The non-social impairments of autism have now become a major focus for cognitive research. One theory proposes dysfunction in executive processes, in an attempt to explain repetitive behaviour and inflexibility. Another theory proposes weak information integration, in an attempt to explain narrow interests and special talents. Autism research has thus stimulated ideas on important mind-brain systems that may be dedicated to the development of social awareness, executive functions and integrative processing.     

PERSONAL CONSTRUCT PSYCHOLOGY AND AUTISM

There has been no significant writing within personal construct psychology about autistic spectrum disorders, despite the fact that this approach provides promising models in a number of other specific areas of human difficulty. This article outlines a PCP model of autism, based on a wide variety of recent research findings and writings, including those of autism sufferers themselves. Autism is considered in the light of Kelly's fundamental postulate and 11 corollaries as well as Procter's (1978) group and family corollaries. It is argued that Kelly's theory provides an integrative framework for considering this complex set of disorders with implications for further research in autism and the early development of social cognition as well as for therapeutic and educational intervention in helping people struggling with autistic spectrum disorders.     

偏向“原理”的钟摆：自闭症共情-系统化理论述评

共情-系统化(Empathizing–Systemizing, E-S)理论是自闭症研究领域中的新兴理论,是对“心盲”理论的扩展。该理论认为自闭症个体的共情缺损,系统化无损甚至超常,并用这两个心理机制全面地解释了自闭症的社交障碍和沟通障碍两种社会性特征以及兴趣狭窄、行为刻板和能力孤岛三种非社会性特征。文章概述了共情-系统化理论的形成过程、证据以及该理论与其它重要理论的关系,并就共情和系统化的关系、共情和系统化的生理基础以及共情-系统化理论对自闭症治疗的启示等问题进行了反思与展望。