Anterior EEG asymmetry and the Modifier Model of Autism.

Individual differences in the expression of autism complicate research on the nature and treatment of this disorder. In the Modifier Model of Autism (Mundy et al. 2007), we proposed that individual differences in autism may result not only from syndrome specific causal processes, but also from variability in generic, non-syndrome specific modifier processes that affect the social and emotional development of all people. One study supporting this model found that measures of resting anterior EEG asymmetry, a measure reflecting complex brain processes associated with generic individual differences in approach and avoidance motivation, may help explain differences in the expression of autism in children without intellectual disabilities (Sutton et al. 2005). In the current study, we partially replicated the observation that children with autism who exhibited a pattern of left frontal EEG asymmetry tended to display milder levels of social symptoms, although in the current sample this pattern applied only to HFA children with relatively lower verbal IQs. New observations indicated that left frontal EEG asymmetry was also associated with retrospective parent reports of significantly later age of onset of symptoms, but also higher levels of self-reported outward expressions of anger as well as symptoms of obsessive compulsive disorder in school-age higher functioning children with ASD. Therefore, the results of this study provide a new and fully independent set of observations, which indicate that individual differences in anterior EEG asymmetry may significantly moderate the expression and developmental course of autism. This observation may have clinical implications for identifying meaningful diagnostic sub-groups among children with autism.

The Modifier Model of Autism and Social Development in Higher Functioning Children.

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 refractor 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 HFA 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.