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The modifier model of autism and social development in higher functioning children

出版社

SAGE PUBLICATIONS INC
DOI: 10.2511/rpsd.32.2.124

关键词

phenotypic variability; comorbity; self-monitoring; motivation and attributional processes; autism

资金

  1. NIMH NIH HHS [R01 MH071273-03, R01 MH071273] Funding Source: Medline

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The study of phenotypic variability in social impairments and comorbid emotional disorders in autism is important because it provides information on phenotypic differences that currently complicate diagnosis, research, and treatment of this disorder Currently, though, relatively little is known about the processes that contribute to individual differences in social impairments and comorbidity in autism. In this paper, we present a model that suggests modifier processes (MPs), which are not necessarily specific to the syndrome, refract or alter the expression of autism and contribute to fundamental behavioral and psychological differences in children diagnosed with this disorder One MPs involves the somewhat surprising tendency of some children with higher functioning autism (HFA) to make attributions about other peoples thoughts, although they have social cognitive deficits. Just as in other children, the attributions of children with HFA are linked to some of their behavioral problems. Another MP involves the influence of differences in motivation associated with the behavioral activation and inhibition systems that can be assessed with measures of anterior EEG asymmetry. This dimension of motivation may be linked to how active but inappropriate and withdrawn children with HFA may appear. Third, differences in the self-monitoring of errors among children with HEA appear to be related to individual differences in IQ and social symptom severity in these children. The possible role of these MPs in diagnostic subgroups and differences in treatment responses among children with HFA are discussed. In addition, the role of MPs in understanding the effects associated with specific genetic functions in autism, such as those associated with the serotonin transporter gene (5-HTTLPR), is discussed. A conclusion of this paper is that the varied expression of autism may require that we understand how autism interacts with other non-syndrome-specific processes that are related to individual differences in all people.

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