Developmental heterochrony and the evolution of autistic perception, cognition and behavior
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Developmental heterochrony and the evolution of autistic perception, cognition and behavior Bernard Crespi
Abstract Background: Autism is usually conceptualized as a disorder or disease that involves fundamentally abnormal neurodevelopment. In the present work, the hypothesis that a suite of core autism-related traits may commonly represent simple delays or non-completion of typical childhood developmental trajectories is evaluated. Discussion: A comprehensive review of the literature indicates that, with regard to the four phenotypes of (1) restricted interests and repetitive behavior, (2) short-range and long-range structural and functional brain connectivity, (3) global and local visual perception and processing, and (4) the presence of absolute pitch, the differences between autistic individuals and typically developing individuals closely parallel the differences between younger and older children. Summary: The results of this study are concordant with a model of ‘developmental heterochrony’, and suggest that evolutionary extension of child development along the human lineage has potentiated and structured genetic risk for autism and the expression of autistic perception, cognition and behavior. Keywords: Autism, Development, Evolution, Heterochrony
Background The autism spectrum is a set of neurodevelopmental conditions characterized and defined by deficits in language and social communication, combined with high expression of restricted interests and repetitive behavior [1,2]. Autism is highly heritable [3], and etiologically heterogeneous, such that a broad range of single-gene, genomic, polygenic and environmental variation has been shown to contribute to the development of a similar, convergent suite of overlapping phenotypes [2,4]. The causes of autism have been studied predominantly using genetic, neurological and psychological conceptualizations and approaches [1,2,4]. The former two approaches have focused on proximate, molecular-genetic, neurodevelopmental, and synaptic causes of autism considered in terms of dysfunctionality and deficits. By contrast, the latter approach commonly involves consideration of both proximate causes and theoretical psychological models of autism-related phenotypes, with autism considered in terms of cognitive or perceptual ‘styles’ or ‘types’, such as weak central coherence [5], high Correspondence: [email protected] Department of Biological Sciences, Simon Fraser University, 8888 University Drive, Burnaby, British Columbia, V5A 1S6, Canada
systemizing relative to empathizing [6], or enhanced perceptual function [7,8]. Such styles are atypical but represent extreme manifestations of normally-distributed variation [9], and comprise both relative deficits (mainly in social cognition) and relative strengths (mainly in non-social perception, cognition and task performance). Evolutionary approaches to the study of autism have been largely restricted to accounts of how phenotypes subject to central deficits in autism, especially language and joint attention
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