Brain development in autism: early overgrowth followed by premature arrest of growth

Due to the relatively late age of clinical diagnosis of autism, the early brain pathology of children with autism has remained largely unstudied. The increased use of retrospective measures such as head circumference, along with a surge of MRI studies of toddlers with autism, have opened a whole new area of research and discovery. Recent studies have now shown that abnormal brain overgrowth occurs during the first 2 years of life in children with autism. By 2-4 years of age, the most deviant overgrowth is in cerebral, cerebellar, and limbic structures that underlie higher-order cognitive, social, emotional, and language functions. Excessive growth is followed by abnormally slow or arrested growth. Deviant brain growth in autism occurs at the very time when the formation of cerebral circuitry is at its most exuberant and vulnerable stage, and it may signal disruption of this process of circuit formation. The resulting aberrant connectivity and dysfunction may lead to the development of autistic behaviors. To discover the causes, neural substrates, early-warning signs and effective treatments of autism, future research should focus on elucidating the neurobiological defects that underlie brain growth abnormalities in autism that appear during these critical first years of life.     

Investigating the role of alexithymia on the empathic deficits found in schizotypy and autism spectrum traits

Alexithymia, the inability to identify and describe one’s emotional experience, is elevated in many clinical populations, and related to poor interpersonal functioning. Alexithymia is also associated with empathic deficits in individuals with autism spectrum disorders. Accordingly, a better understanding of alexithymia could elucidate the nature of social-cognitive deficits transdiagnostically. We investigated alexithymia and components of empathy in relation to schizotypal and autism spectrum traits in healthy college students. Specifically, we examined higher-order components of empathic processing that involve perspective taking and other-oriented concern, which are reduced in alexithymia.Higher-order empathic processing was inversely correlated with both schizotypal and autism spectrum traits. Bootstrapping techniques revealed that alexithymia had a significant indirect effect on the relationship between higher-order empathy and these personality traits; thus, alexithymia contributes uniquely to their relationship. These findings suggest alexithymia represents one possible mechanism for the development of empathic deficits in these populations.These results are consistent with the perspective that awareness of one’s own emotional state may predicate a successful empathic response to another’s. This work highlights the importance of a consideration of alexithymia in elucidating the nature of empathic deficits in various clinical populations, and points to a potential point of social intervention.     

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.     

Emulation and mimicry for social interaction: a theoretical approach to imitation in autism

The "broken-mirror" theory of autism argues that dysfunction of the "mirror neuron system" is a root cause of social disability in autism. The present paper aims to scrutinize this theory and, when it breaks down, to provide an alternative. Current evidence suggests that children with autism are able to understand and emulate goal-directed actions, but may have specific impairments in automatic mimicry of actions without goals. These data are not compatible with the broken-mirror theory, but can be accounted for by a new model called EP-M. The EP-M model segments the mirror neuron system into an indirect, parietal route for goal emulation and planning (EP) and a direct occipital-frontal route for mimicry (M). This fractionation is consistent with neuroimaging and behavioural studies of the mirror neuron system in typical children and adults. I suggest that top-down modulation of the direct M route may be dysfunctional in individuals with autism, leading to abnormal behaviours on mimicry tasks as well as other social disabilities.     

Early processing of emotional faces in children with autism: An event-related potential study

Social deficits are one of the most striking manifestations of autism spectrum disorders (ASDs). Among these social deficits, the recognition and understanding of emotional facial expressions has been widely reported to be affected in ASDs. We investigated emotional face processing in children with and without autism using event-related potentials (ERPs). High-functioning children with autism (n = 15, mean age = 10.5 ± 3.3 years) completed an implicit emotional task while visual ERPs were recorded. Two groups of typically developing children (chronological age-matched and verbal equivalent age-matched [both ns = 15, mean age = 7.7 ± 3.8 years]) also participated in this study. The early ERP responses to faces (P1 and N170) were delayed, and the P1 was smaller in children with autism than in typically developing children of the same chronological age, revealing that the first stages of emotional face processing are affected in autism. However, when matched by verbal equivalent age, only P1 amplitude remained affected in autism. Our results suggest that the emotional and facial processing difficulties in autism could start from atypicalities in visual perceptual processes involving rapid feedback to primary visual areas and subsequent holistic processing.     

Sub‐threshold autism traits: The role of trait emotional intelligence and cognitive flexibility

Theory and research suggests that features of autism are not restricted to individuals diagnosed with autism spectrum disorders (ASDs), and that autism‐like traits vary throughout the general population at lower severities. The present research first investigated the relationship of autism traits with trait emotional intelligence and empathy in a sample of 163 adults aged between 18 and 51 years (44% male). It then examined performance on a set of tasks assessing social cognition and cognitive flexibility in 69 participants with either high or low scores on ASD traits. Results confirm that there is pronounced variation within the general population relating to ASD traits, which reflect similar (though less severe) social‐cognitive and emotional features to those observed in ASDs.     

Backward masking: evidence of reduced subcortical amygdala engagement in autism

Recent data suggest that subthreshold presentation of emotional information is relayed to the amygdala along subcortical pathways. We examined the effect of backward masked neutral and anxious faces on the social decisions of a group of high functioning children with autism ages 7-13 years and matched controls. Participants were asked to select the friendliest of two faces, one of which was associated with the subthreshold (33 ms) presentation of an anxious face (A/N) and the other a subthreshold neutral face (N/N). Neutral paired faces were selected more often than A/N paired faces by both groups. However, children with autism selected significantly fewer N/N stimuli and more A/N stimuli than controls. These results suggest that the social choices of children with autism were influenced less by emotional information presented subconsciously and suggest a subcortical contribution to the social/emotional processing deficits observed in autism.     

Expressive drawing ability in children with autism

The autistic impairments in emotional and social competence, imagination and generating ideas predict qualitative differences in expressive drawings by children with autism beyond that accounted by any general learning difficulties. In a sample of 60 5–19‐year‐olds, happy and sad drawings were requested from 15 participants with non‐savant autism and compared with those drawn by three control groups matched on either degree of learning difficulty (MLD), mental age (MA) or chronological age (CA). All drawings were rated by two artists on a 7‐point quality of expression scale. Contrary to our predictions, the drawings from the autistic group were rated similar to those of the MA and MLD groups. Analysis of the people and social content of the drawings revealed that although children with autism did not draw fewer people, they did draw more immature forms than mental age controls. Furthermore, there was tentative evidence that fewer social scenes were produced by the autism sample. We conclude that the overall merit of expressive drawing in autism is commensurate with their general learning difficulties, but the social/emotional impairment in autism affects their drawings of people and social scenes.     

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。     

从“变色龙效应”到“镜像神经元”再到“模仿过多症”—— 作为社会交流产物的人类无意识模仿

人类无意识模仿是指人们在社会交流时会相互无意识地模仿对方的一些动作、表情和行为方式。其在个体社会认知以及人际交流上扮演着重要的角色。通过回顾近十年来人类无意识模仿的各个领域内的研究进展, 以及分析无意识模仿的行为学效应, 脑神经机制以及病理学调控, 可以得出如下结论：所有神经层面以及行为层面的人类无意识模仿现象都是社会交流的产物。该观点在澄清无意识模仿神经机制以及促进幼儿社会认知发展方面具有一定启示意义, 而探索孤独症患者无意识模仿障碍的病理机制有望为该领域的未来研究开启新的方向。     

Neural correlates of coherent and biological motion perception in autism

Recent evidence suggests those with autism may be generally impaired in visual motion perception. To examine this, we investigated both coherent and biological motion processing in adolescents with autism employing both psychophysical and fMRI methods. Those with autism performed as well as matched controls during coherent motion perception but had significantly higher thresholds for biological motion perception. The autism group showed reduced posterior Superior Temporal Sulcus (pSTS), parietal and frontal activity during a biological motion task while showing similar levels of activity in MT+/V5 during both coherent and biological motion trials. Activity in MT+/V5 was predictive of individual coherent motion thresholds in both groups. Activity in dorsolateral prefrontal cortex (DLPFC) and pSTS was predictive of biological motion thresholds in control participants but not in those with autism. Notably, however, activity in DLPFC was negatively related to autism symptom severity. These results suggest that impairments in higher-order social or attentional networks may underlie visual motion deficits observed in autism.     

Face processing in different brain areas,and critical band masking

Neurophysiological evidence is described showing that some neurons in the macaque inferior temporal visual cortex have responses that are invariant with respect to the position, size, view, and spatial frequency of faces and objects, and that these neurons show rapid processing and rapid learning. Critical band spatial frequency masking is shown to be a property of these face‐selective neurons and of the human visual perception of faces. Which face or object is present is encoded using a distributed representation in which each neuron conveys independent information in its firing rate, with little information evident in the relative time of firing of different neurons. This ensemble encoding has the advantages of maximizing the information in the representation useful for discrimination between stimuli using a simple weighted sum of the neuronal firing by the receiving neurons, generalization, and graceful degradation. These invariant representations are ideally suited to provide the inputs to brain regions such as the orbitofrontal cortex and amygdala that learn the reinforcement associations of an individual's face, for then the learning, and the appropriate social and emotional responses generalize to other views of the same face. A theory is described of how such invariant representations may be produced by self‐organizing learning in a hierarchically organized set of visual cortical areas with convergent connectivity. The theory utilizes either temporal or spatial continuity with an associative synaptic modification rule. Another population of neurons in the cortex in the superior temporal sulcus encodes other aspects of faces such as face expression, eye‐gaze, face view, and whether the head is moving. These neurons thus provide important additional inputs to parts of the brain such as the orbitofrontal cortex and amygdala that are involved in social communication and emotional behaviour. Outputs of these systems reach the amygdala, in which face‐selective neurons are found, and also the orbitofrontal cortex, in which some neurons are tuned to face identity and others to face expression. In humans, activation of the orbitofrontal cortex is found when a change of face expression acts as a social signal that behaviour should change; and damage to the human orbitofrontal and pregenual cingulate cortex can impair face and voice expression identification, and also the reversal of emotional behaviour that normally occurs when reinforcers are reversed.     

A comparison of behavioral and emotional functioning in children and adolescents with Autistic Disorder and PDD-NOS.

Behavioral symptomatology was compared in 26 children and adolescents with Autistic Disorder ("autism") and 25 children and adolescents with Pervasive Developmental Disorder, Not Otherwise Specified ("PDD-NOS"). Relative to individuals with PDD-NOS, those with autism had more symptoms of depression, social withdrawal, atypical behavior, and immature social skills--and fewer family problems. These differences remained even when group differences in intellectual ability were statistically controlled. No group differences emerged in somatization, anxiety, or hyperactivity. Findings suggest that although both groups demonstrate considerable evidence of behavioral and emotional problems, those with autism are at particularly high risk for comorbid behavioral and emotional disabilities.     

孤独症儿童的情绪共情能力及情绪表情注意方式

研究探讨了孤独症儿童的情绪共情能力及情绪表情注意方式的特点。各选取15名孤独症儿童以及作为对照组的智力障碍儿童和普通儿童各15名, 完成情绪共情实验, 同时使用生物反馈仪记录自主生理反应, 眼动仪记录眼动轨迹。结果发现孤独症儿童对情绪表情的自动模仿及感知能力显著低于智力障碍儿童与普通儿童; 对面孔的总注视时间、总注视点数均显著少于智力障碍儿童、普通儿童; 对眼部、嘴部的注视时间比及注视点数比均显著低于普通儿童; 对高兴和悲伤表情的注意较多而对恐惧则较少。这提示孤独症儿童的情绪共情能力不足、对情绪表情的注意方式异常。     

fNIRS在自闭症脑功能研究中的应用与展望

社会交往能力是人类生存的基本技能。社交能力的缺失会导致严重的行为障碍和精神疾病,如自闭症。由于自闭症儿童的特殊性,绝大多数的自闭症脑成像研究多集中在年龄较大的高功能自闭症儿童在静息态或简单的任务态下的脑激活模式或功能连接状态。自闭症的核心症状—社会交往障碍和语言交流障碍却较少有研究触及。近年来,近红外光学脑功能成像技术的发展为我们在真实的交流和互动中研究自闭症儿童的神经病理机制提供了新的工具和机遇。     

An examination of the structural, discriminant, nomological, and incremental predictive validity of the MSCEIT© V2.0

We examined the structural, discriminant, nomological, and incremental predictive validity of a behavioral measure of emotional intelligence, using data from two undergraduate student samples. Covariance structure modeling indicated that the eight subscales of the MSCEIT© V2.0 were best modeled with a solution consisting of three first-order factors, and supported the existence of one higher-order factor of overall emotional intelligence. Multi-group confirmatory factor analyses indicated that the higher-order factor had discriminant validity from personality and conformity. Contrary to prediction, the higher-order factor was more highly correlated to social desirability than to general mental ability or long term affect. Finally, hierarchical regression results indicated that overall emotional intelligence did not predict incremental variance in either GPA or life satisfaction.     

Within- and between-nervous-system inhibition of return: Observation is as good as performance

Inhibition of return (IOR) has been shown to occur when an individual returns to a target location (within-person IOR) and when an individual moves to a location just engaged by another individual (between-person IOR). Although within- and between-person IOR likely result from the same inhibitory mechanisms, different processes must activate these mechanisms following the performance and observation of action. Consistent with the suggestion that the mirror neuron system may be responsible for activating the inhibitory mechanisms behind IOR on observation trials, between-person IOR was only detected under restricted viewing conditions known to activate mirror neurons. These results indicate that mirror neuron system may be involved in both higher-order and automatic cognitive behavior.     

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     

Plasticity of nonneuronal brain tissue: roles in developmental disorders

Neuronal and nonneuronal plasticity are both affected by environmental and experiential factors. Remodeling of existing neurons induced by such factors has been observed throughout the brain, and includes alterations in dendritic field dimensions, synaptogenesis, and synaptic morphology. The brain loci affected by these plastic neuronal changes are dependent on the type of experience and learning. Increased neurogenesis in the hippocampal dentate gyrus is a well-documented response to environmental complexity ("enrichment") and learning. Exposure to challenging experiences and learning opportunities also alters existing glial cells (i.e., astrocytes and oligodendrocytes), and up-regulates gliogenesis, in the cerebral cortex and cerebellum. Such glial plasticity often parallels neuronal remodeling in both time and place, and this enhanced morphological synergism may be important for optimizing the functional interaction between glial cells and neurons. Aberrant structural plasticity of nonneuronal elements is a contributing factor, as is aberrant neuron plasticity, to neurological and developmental disorders such as epilepsy, autism, and mental retardation (i.e., fragile X syndrome). Some of these nonneuronal pathologies include abnormal cerebral and cerebellar white matter and myelin-related proteins in autism; abnormal myelin basic protein in fragile X syndrome (FXS); and abnormal astrocytes in autism, FXS, and epilepsy. A number of recent studies demonstrate the possibility of using environmental and experiential intervention to reduce or ameliorate some of the neuronal and nonneuronal abnormalities, as well as behavioral deficits, present in these neurological and developmental disorders.