ISSN 1671-3710
CN 11-4766/R
主办:中国科学院心理研究所
出版:科学出版社

心理科学进展 ›› 2021, Vol. 29 ›› Issue (7): 1239-1250.doi: 10.3724/SP.J.1042.2021.01239

• 研究前沿 • 上一篇    下一篇

孤独症儿童动作发展障碍的神经机制

王琳, 王志丹(), 王泓婧   

  1. 江苏师范大学教育科学学院, 徐州 221116
  • 收稿日期:2019-09-15 出版日期:2021-07-15 发布日期:2021-05-24
  • 基金资助:
    江苏省高等学校自然科学研究项目资助(19KJB190002);2020年度江苏师范大学研究生科研创新项目(2020 XKT227)

The neural mechanisms of developmental motor disorders in children with autism spectrum disorder

WANG Lin, WANG Zhidan(), WANG Hongjing   

  1. School of Education Science, Jiangsu Normal University, Xuzhou 221116, China
  • Received:2019-09-15 Online:2021-07-15 Published:2021-05-24

摘要:

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。

关键词: 孤独症谱系障碍, 儿童, 动作发展障碍, 神经机制

Abstract:

Developmental motor disorders, one of common features of autism spectrum disorder (ASD), are significantly related to the social deficits and the severity of core symptoms of ASD. Previous studies have gradually confirmed that developmental motor disorders are a part of the overall brain dysfunction in children with ASD and share the common neural basis with the core symptoms of ASD.

Through a systematic review of the neuroscience literature, we found that the neural mechanism of developmental motor disorders in children with ASD included changes in neurobiochemical mechanisms, fundamental parts of brain structure and brain function mechanisms. Firstly, the neurobiochemical mechanism involved the alteration in the concentration of GABA and of 5-HT, and the abnormal expression of GABA-related protein and of shank protein. The alteration in the concentration of GABA was related to the abnormality of cortical inhibitory function that stimulated sense and motor. The abnormal expression of shank protein was related to cerebellar motor dysfunction. The alteration in the concentration of 5-HT and the abnormal expression of shank protein were related to motor learning difficulty. Secondly, fundamental parts of brain structure involved abnormalities in the structure of the cerebellum, basal ganglia, and corpus callosum. The abnormality in the structure of cerebellum hindered the ability of motor adaptability and motor learning. The abnormality in the structure of basal ganglia was related to motor control problems and gait deviation. The abnormality in the structure of corpus callosum was likely to affect the development of motor coordination. Thirdly, the brain function mechanisms involved the abnormalities in cerebellar activation, cortical-cerebellar circuits and brain connections, and lateralization of brain function. The abnormality in cerebellar activation explained the motor execution difficulty. The abnormality in cortical-cerebellar circuits was related to the difficulty in forming complex movement patterns during motor learning. The lateralization of brain function might be the basis of the gross motor development. The abnormal brain connections were related to the motor execution difficulty, the motor coordination disorder, and the sensory-motor dysfunction.

Overall, The above three mechanisms did not operate independently, but to be an interconnected organic entity. Specifically, the neurobiochemical mechanisms led to not only the defects of the development of the central nervous system, but also the synaptic excitation/ inhibition imbalance, thus in turn resulting in the changes of the functional connectivity between cerebellum and motor cortex in children with ASD. The fundamental parts of brain structure had a negative impact on the whole-brain connectivity in children with ASD. The former two together triggered the brain function mechanisms of children with ASD, which ultimately resulted in developmental motor disorders.

Besides, the common neural basis shared by the developmental motor disorders and the core symptoms of ASD mainly included the mirror neuron dysfunction, the abnormalities of the thalamus, the basal ganglia, the cerebellum and the mutations of SLC7A5 and PTEN in children with ASD: social and motor deficits of ASD might be caused by the abnormality in the mirror neuron system; the abnormalities of the thalamus, the basal ganglia, and the cerebellum were related not only to the developmental motor disorders, but also to the core symptoms of ASD; the mutations of SLC7A5 and PTEN were expected to serve as a breakthrough linking social deficits and developmental motor disorders in the field of genetics.

Future research are expected to focus on other neurotransmitters closely related to motor, such as acetylcholine and dopamine, to explore the dynamic mechanism and formation of the neural network of developmental motor disorders, and to analyze the interaction between the underlying neural mechanisms of developmental motor disorders and that of core symptoms of autism.

Key words: autism spectrum disorders, children, developmental motor disorders, neural mechanism

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