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.     

Cognitive deficits in developmental disorders

The existence of specific developmental disorders such as dyslexia and autism raises interesting issues about the structure of the normally developing mind. In these disorders distinct cognitive deficits can explain a range of behavioural impairments and have the potential to be linked to specific brain abnormalities. One possibility is that there are specific mechanisms dedicated to particular types of information processing. These mechanisms may function independently of more general information processing systems and may have a distinct anatomical basis in the brain.     

从心理理论与执行功能的关系看孤独症

孤独症是一种病因未明的广泛性发展障碍,它的诊断主要基于患者的行为表现。针对这些行为特点,研究者们提出了心理理论缺失说和执行功能障碍说。但是,有研究表明孤独症患者并不是在所有的心理理论任务和执行功能任务上都存在障碍。所以,单纯地采用心理理论缺失说或执行功能障碍说都不能完整解释孤独症症状。一般来说,心理理论缺失的孤独症个体,同时也伴有执行功能障碍。近年来,大量的研究结果发现,心理理论与执行功能确实存在紧密联系。然而,目前对它们关系的考察主要集中在学龄前儿童的错误信念理解和抑制控制上。心理理论与执行功能都分别包含许多成分,它们彼此的关系可能会在不同年龄段发生变化。因此,研究者需要进一步探查不同年龄段,不同心理理论任务与执行功能不同成分与范式之间的关系,并将这种关系应用于临床实践,帮助诊断和培训孤独症个体。     

自闭症儿童的心理理论与中心信息整合的关系探讨

自闭症儿童的心理理论一直是儿童心理理论研究的重要领域,自闭症儿童身上心理理论缺失这一领域特殊性的加工缺损与弱的中心信息整合这一领域一般性的加工异常之问的关系研究逐渐受到了广泛关注。在阐述自闭症领域的心理理论研究,并介绍弱的中心信息整合理论的基本观点和实验证据之后,在此探讨了两者之间的关系,包括两者相互独立的观点、相互关联的观点以及其他的不同观点,并对今后的研究方向做出了展望。     

Religious Cognition and Behaviour in Autism: The Role of Mentalizing

Mentalizing, or theory of mind, has been argued to be critical for supporting religious beliefs and practices involving supernatural agents. As individuals with autism spectrum conditions have been found to have deficits in mentalizing, this raises the question as to how they may conceive of gods and behave in relation to gods. To examine this, we compared high-functioning individuals with autism spectrum conditions (HFA) to typically developing individuals across seven key aspects of religious cognition and behaviour: (a) strength of belief, (b) anthropomorphism of god concepts, (c) felt closeness toward the god, (d) prayer habits, (e) attraction to prayer, (f) efficacy of prayer, and (g) a sense of agency while praying. A battery of mentalizing tasks was administered to measure mentalizing ability, along with the Autism-Spectrum Quotient. As expected, typically developing subjects performed better than HFA subjects in the advanced mentalizing task. However, no statistically significant differences were found with first-order and second-order false belief tasks. In contrast to our predictions and previous research on the religiosity of HFA, we found very little differences between the groups in their religious cognition and behaviour. Moreover, the relationship between mentalizing ability and most of our measures of religious cognition and behaviour was weak and negative. Our data suggest that HFA's deficits in mentalizing appear to have only minimal impact on the way they interact and think about gods. We end the article by reevaluating the role mentalizing may have in religious cognition and behaviour.     

孤独症生命早期脑过度生长现象及启示

孤独症神经结构研究中近来一个重要的发现是,孤独症生命早期存在脑过度生长的现象。进一步的探查表明,孤独症个体脑的过度生长主要由脑白质的过度生长造成,并且脑的过度生长又主要体现于那些较晚成熟的高级脑区。这一研究成果有助于孤独症儿童的早期发现和诊断,也提示孤独症并不是由单一的局部神经缺陷造成,其存在着广泛分布式的神经发展障碍     

Social cognition and its neural correlates in schizophrenia and autism

The study of social cognition in psychiatric disorders has become increasingly popular in recent years. This is due to the its proposed link to social functioning and the inability of general neurocognitive skills to explain the spectrum of impairments observed in patients. This article reviews research into two of the processes thought to underlie social cognition (emotion perception and theory of mind) in schizophrenia and autism. This is followed by a look at neuroimaging studies and their efforts to localize the neural correlates of emotion perception and theory of mind in the two disorders. We concluded that while a specific impairment in emotion perception and theory of mind skills cannot be generalized to all individuals with autism and schizophrenia, there are subpopulations that have lingering deficits of social cognition tasks. Neuroimaging work consistently points to the involvement of the fusiform gyrus and amygdala in emotion processing, while the medial prefrontal and frontal cortex are implicated in tasks invoking theory of mind. We propose that deficits of social cognition may benefit from cognitive remediation therapy and pharmacological cognitive enhancers.     

MINDS, INTRINSIC PROPERTIES, AND MADHYAMAKA BUDDHISM

Certain philosophers and scientists have noticed that there are data that do not seem to fit with the traditional view known as the Mind/Brain Identity theory (MBI). This has inspired a new theory about the mind known as the Hypothesis of Extended Cognition (HEC). Now there is a growing controversy over whether these data actually require extending the mind out beyond the brain. Such arguments, despite their empirical diversity, have an underlying form. They all are disputes over where to draw the line between intrinsic and relational causal powers. The second-century Buddhist philosopher Nagarjuna deals with similar issues when he argues for a middle way between the two positions that were known in his time by the terms eternalism and nihilism. Eternalism, like MBI, asserts that the mind is a permanent enduring substance (although the two theories disagree as to how long mind endures). Nihilism argued that the mind had no intrinsic existence, and today some argue that HEC could lead us to a similar conclusion. Nagarjuna's argument for a middle way between these two extremes is similar to an argument that can be made for HEC. We can accept that neither the brain nor any other single physical item is identical to the mind without falling down the slippery slope that leads to "The mind does not really exist, and therefore we are one with everything." Nagarjuna was correct to say that the mind has conventional reality—that the mind exists even though there is no sharp border between the mind and the world.     

Performance-based measures in autism: implications for diagnosis, early detection, and identification of cognitive profiles

Provides a critical review of performance-based assessment measures in autism. Currently, performance-based measures of autism are being explored in two domains: structured play sessions and cognitive-neuropsychological assessments. Structured play sessions are designed to elicit the behavioral symptoms associated with autism to provide a consistent and valid means of early detection and diagnosis of autism across different evaluators and settings. These structured play sessions provide a supplement to diagnostic instruments based on parental report. Cognitive-neuropsychological tasks have been used to identify possible underlying cognitive impairments in autism including executive function, theory of mind, selective attention, and abstraction. Currently, cognitive tasks are useful in treatment planning but are inappropriate for diagnostic purposes. Important goals for the future will be to integrate parent-report diagnostic interviews and structured play observations and to identify a profile of cognitive impairments that are specific to pervasive developmental disorders that can be incorporated into diagnostic protocols.     

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.     

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。     

Failure to deactivate in autism: the co-constitution of self and other

A new brain imaging study demonstrates that patients with autism have a strikingly different pattern of brain activity compared with control subjects. During cognitive tasks, cortical areas known as the "default state" network--areas that have been implicated in both self-referential processing and processing of socially relevant information--typically reduce their brain activity. In patients with autism, such a reduction was not observed. This new finding indicates that a core deficit in autism might be related to the construal of a sense of self in its relationship with others and will certainly generate exciting new research on the neurobiology of autism.     

Toward a developmental neurobiology of autism

Autism is a complex, behaviorally defined, developmental brain disorder with an estimated prevalence of 1 in 1,000. It is now clear that autism is not a disease, but a syndrome with a strong genetic component. The etiology of autism is poorly defined both at the cellular and the molecular levels. Based on the fact that seizure activity is frequently associated with autism and that abnormal evoked potentials have been observed in autistic individuals in response to tasks that require attention, several investigators have recently proposed that autism might be caused by an imbalance between excitation and inhibition in key neural systems including the cortex. Despite considerable ongoing effort toward the identification of chromosome regions affected in autism and the characterization of many potential gene candidates, only a few genes have been reproducibly shown to display specific mutations that segregate with autism, likely because of the complex polygenic nature of this syndrome. Among those, several candidate genes have been shown to control the early patterning and/or the late synaptic maturation of specific neuronal subpopulations controlling the balance between excitation and inhibition in the developing cortex and cerebellum. In the present article, we review our current understanding of the developmental mechanisms patterning the balance between excitation and inhibition in the context of the neurobiology of autism.     

Autism Overflows: Increasing Prevalence and Proliferating Theories

This selective review examines the lack of an explanation for the sharply increasing prevalence of autism, and the lack of any synthesis of the proliferating theories of autism. The most controversial and most widely disseminated notion for increasing prevalence is the measles–mumps–rubella/thimerosal vaccine theory. Less controversial causes that have been proposed include changes in autism diagnostic criteria, increasing services for autism, and growing awareness of the disorder. Regardless of its causes, the increasing prevalence of autism has put pressure on the field of autism research to generate productive and predictive theories of autism. However, the heterogeneity of brain deficits, impaired behaviors, and genetic variants in autism have challenged researchers and theorists, and despite 45 years of research, no standard causal synthesis has emerged. Research going forward should assume that autism is an aggregation of myriad independent disorders of impaired sociality, social cognition, communication, and motor and cognitive skills.     

Serotonin in autism and pediatric epilepsies

Serotonergic abnormalities have been reported in both autism and epilepsy. This association may provide insights into underlying mechanisms of these disorders because serotonin plays an important neurotrophic role during brain development--and there is evidence for abnormal cortical development in both autism and some forms of epilepsy. This review explores the hypothesis that an early disturbance in the serotonin system affects cortical development and the development of thalamocortical innervation, and is a potential mechanism, common to autism and pediatric epilepsies associated with cortical dysplasia. An argument is made that cortical malformation leads to abnormalities of thalamocortical connectivity, and that serotonin plays a critical role in this process. Finally, a role for altered metabolism of the serotonin precursur, tryptophan, in both epilepsy and autism is discussed.     

Functional connectivity differences in autism during face and car recognition: underconnectivity and atypical age‐related changes

Face recognition abilities improve between adolescence and adulthood over typical development (TD), but plateau in autism, leading to increasing face recognition deficits in autism later in life. Developmental differences between autism and TD may reflect changes between neural systems involved in the development of face encoding and recognition. Here, we focused on whole‐brain connectivity with the fusiform face area (FFA), a well‐established face‐preferential brain region. Older children, adolescents, and adults with and without autism completed the Cambridge Face Memory Test, and a matched car memory test, during fMRI scanning. We then examined task‐based functional connectivity between the FFA and the rest of the brain, comparing autism and TD groups during encoding and recognition of face and car stimuli. The autism group exhibited underconnectivity, relative to the TD group, between the FFA and frontal and primary visual cortices, independent of age. Underconnectivity with the medial and rostral lateral prefrontal cortex was face‐specific during encoding and recognition, respectively. Conversely, underconnectivity with the L orbitofrontal cortex was evident for both face and car encoding. Atypical age‐related changes in connectivity emerged between the FFA and the R temporoparietal junction, and R dorsal striatum for face stimuli only. Similar differences in age‐related changes in autism emerged for FFA connectivity with the amygdala across both face and car recognition. Thus, underconnectivity and atypical development of functional connectivity may lead to a less optimal face‐processing network in the context of increasing general and social cognitive deficits in autism.     

Links between theory of mind and executive function in young children with autism: clues to developmental primacy

There has been much theoretical discussion of a functional link between theory of mind (ToM) and executive function (EF) in autism. This study sought to establish the relationship between ToM and EF in young children with autism (M = 5 years, 6 months) and to examine issues of developmental primacy. Thirty children with autism and 40 typically developing children, matched on age and ability, were assessed on a battery of tasks measuring ToM (1st- and 2nd-order false belief) and components of EF (planning, set shifting, inhibition). A significant correlation emerged between ToM and EF variables in the autism group, independent of age and ability, while ToM and higher order planning ability remained significantly related in the comparison group. Examination of the pattern of ToM-EF impairments in the autism group revealed dissociations in 1 direction only: impaired ToM with intact EF. These findings support the view that EF may be 1 important factor in the advancement of ToM understanding in autism. The theoretical implications of these findings are discussed.     

The Implications of Brain Connectivity in the Neuropsychology of Autism

Autism is a neurodevelopmental disorder that has been associated with atypical brain functioning. Functional connectivity MRI (fcMRI) studies examining neural networks in autism have seen an exponential rise over the last decade. Such investigations have led to the characterization of autism as a distributed neural systems disorder. Studies have found widespread cortical underconnectivity, local overconnectivity, and mixed results suggesting disrupted brain connectivity as a potential neural signature of autism. In this review, we summarize the findings of previous fcMRI studies in autism with a detailed examination of their methodology, in order to better understand its potential and to delineate the pitfalls. We also address how a multimodal neuroimaging approach (incorporating different measures of brain connectivity) may help characterize the complex neurobiology of autism at a global level. Finally, we also address the potential of neuroimaging-based markers in assisting neuropsychological assessment of autism. The quest for a neural marker for autism is still ongoing, yet new findings suggest that aberrant brain connectivity may be a promising candidate.     

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。     

Psychological processes and paranoia: implications for forensic behavioural science

Paranoid delusions have recently become the focus of empirical research. In this article, we review studies of the psychological mechanisms that might be involved in paranoid thinking and discuss their implications for forensic behaviour science. Paranoia has not been consistently associated with any specific neuropsychological abnormality. However, evidence supports three broad types of mechanism that might be involved in delusional thinking in general and paranoia in particular: anomalous perceptual experiences, abnormal reasoning, and motivational factors. There is some evidence that paranoia may be associated with hearing loss, and good evidence that paranoid patients attend excessively to threatening information. Although general reasoning ability seems to be unaffected, there is strong evidence that a jumping- to-conclusions style of reasoning about data is implicated in delusions in general, but less consistent evidence specifically linking paranoia to impaired theory of mind. Finally, there appears to be a strong association between paranoia and negative self-esteem, and some evidence that attempts to protect self-esteem by attributing negative events to external causes are implicated. Some of these processes have recently been implicated in violent behaviour, and they therefore have the potential to explain the apparent association between paranoid delusions and offending.