Abstract
AbstractAutism is a development disorder that is characterized by a significant disturbance of social development. Research strongly suggests that this disorder results from neurological anomalies or deficits. However, both the specific neural systems involved in autism, and the most pertinent behavioral functions of those systems remains unclear. One current topic of debate concerns the degree to which the social disturbance of autism may result from developmental anomalies in neurological systems that subserve cognitive, or affective processes. In this paper a model of the neurological, cognitive, and affective processes involved in the pathogenesis of autism will be described in the context of an attempt to understand dissociations in the early social-skill development of these children. Young children with autism are better able to use social-communication gestures to request objects or events than they are able to use similar gesture simply to initiate joint or socially shared attention relative to an object or event. An integration of recent research suggests that joint attention skill development differs from requesting skill development with regard to affective and cognitive processes that may be associated with frontal and midbrain neurological systems. In particular, this integration of the literature suggests the following: (a) there is a specific neurological subsystem that regulates and promotes what are called social-emotional approach behaviors; (b) the tendency to initiate joint attention bids is prototypical of a social-emotional approach behavior; and (c) attenuation of social-approach behaviors in children with autism leads to a specific impoverishment of social information processing opportunities. This impoverishment has a lifelong negative effect on the social cognitive development of these children.
Publisher
Cambridge University Press (CUP)
Subject
Psychiatry and Mental health,Developmental and Educational Psychology
Cited by
310 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献