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There are two current impediments for genetic and neuroscience research in autism. First, there is no standard comprehensive model of the brain circuits and neurochemistry regulating human social behaviors (Beer & Ochsner, 2006). Second, there is as yet no mapping of gene to brain function to phenotypic expression for component skills of human social behavior (Insel & Fernald, 2004; Panksepp, 2006). Although a complete neural framework for the range of human social skills does not yet exist, research in social neuroscience has led researchers and theorists to construct models of the brain bases of social skills (Adolphs, 2002; Allman et al., 2002; Brothers, 2002; Davidson & Irwin, 2002; Erikson & Shulkin, 2003; Harmon-Jones, 2003; LaBar & Cabeza, 2006; Matthews et al., 2002; Meltzoff & Prinz, 2002; Panksepp, 2006; Porges, 2003; Posamentier & Abdi, 2003; Raichle, 2003; Rapcsak, 2003; Reich et al., 2003; Rolls, 1999; Royzman et al., 2003; Singer et al., 2004). Moreover, although there is no gene—brain—phenotype map for social behaviors, social neuroscience research models do suggest possible links between brain circuits and endophenotype component skills for complex social behavior.
This chapter constructs a component model of the brain bases of social skill from current social neuroscience findings. Three questions are addressed:
To what extent are human social behaviors innately determined?
What brain circuits and component skills for complex social behavior have been proposed?
What do these proposed brain circuits and component skills for complex social behavior tell us about the components of the diagnostic phenotype of autism?
Executive functioning was investigated in 34 children (24 boys and 10 girls) with developmental language disorder (DLD) and 21 children (18 boys and 3 girls) with high-functioning autistic disorder (HAD) matched on Full Scale IQ, Nonverbal IQ, age (mean age 9 year, 1 month), and SES. The DLD group had a Verbal IQ that was 10 points higher than the HAD group. These children were given the Wisconsin Card Sorting Test (WCST), the Mazes subtest from the WISC-R, the Underlining test, and the Rapid Automatized Naming test. In addition, these children were given the Vineland Scales of Adaptive Functioning and the Wing Diagnostic Symptom Checklist in order to assess severity of autistic symptomatology. Results indicated that the only significant difference between the two groups on the cognitive tasks was perseverative errors on the WCST; there was no significant difference on total number of categories achieved or total number of errors on the WCST or on the other executive function measures. There was also significant overlap in the scores between the two groups and the difference in perseverative errors was no longer significant when Verbal IQ was partialled out. Executive functioning was strongly related to all IQ variables in the DLD group and particularly related to Verbal IQ in the HAD group. Although there was a relationship in the HAD group between executive functioning and adaptive functioning, as well as between executive functioning and autistic symptomatology, these relationships were generally no longer significant in the HAD group after the variance due to Verbal IQ was accounted for. The results are interpreted to indicate that although impaired executive functioning is a commonly associated feature of autism, it is not universal in autism and is unlikely to cause autistic behaviors or deficits in adaptive function.