A Novel Framework for Impaired Imitation in ASD

项目总结

Project Summary There is long-standing recognition that people with autism spectrum disorders (ASD) have difficulty imitating others’ actions; some investigators have highlighted impaired imitation as being a core contributor to the development of autism. What is yet unknown is precisely how imitation in children with ASD differs from that of typically developing peers. Following an in-depth review of videos of children imitating, we have identified a task parameter that separates preserved from impaired gesture imitation in ASD: children with ASD have difficulty imitating when the task requires two separate movement elements be coordinated simultaneously. By contrast, imitation is relatively preserved when movement elements are performed serially. The coordination of simultaneous movements is a hallmark of actions performed in the real world. With an eye to optimizing common therapies that depend heavily on imitation, the next step is to tease apart where, in the chain from perception to action, the capacity limitation in simultaneous processing lies. To do this, we propose a rigorous research plan that encompasses three complementary experimental techniques. The first is psychophysical task manipulation: In Aim 1, we will control for a potential confound (total number of gestures). In Aim 2, we will specifically examine the perceptual contribution to simultaneity limitations in ASD, by minimizing the required motor output. The second technique is correlation with relevant clinical neuropsychological measures: In Aim 1, we will examine, within the ASD group, the association between the performance cost of simultaneous (vs. serial) imitation and a clinical measure of praxis/imitative function. We will also assess the relationship between simultaneity cost and certain aspects of social function in ASD that may depend on the simultaneous processing of multiple perceptual items and response plans. In Aim 2, we will examine the relationship between attentional demands in simultaneous imitation and clinical measures of divided attention. The third experimental technique is EEG: Based on published results from our laboratory and others, we hypothesize that simultaneous processing demands will be characterized by an increased magnitude of task-related modulation of EEG activity (event-related synchronization/desynchronization: ERS/ERD) in controls. By examining for limitations of this effect in ASD, in either motor or visual networks, or both, we can assess the locus of capacity limitation. By better understanding the relative contributions of perceptual and motor processes, we can optimize the critical therapies in ASD that depend on imitation. Further, by better characterizing the underlying physiology, we open a path to neuro-stimulatory therapies. If, as Rogers and Pennington (1991) suggest, imitation is key to successful vs. aberrant development in children prone to ASD, the application of such therapies in a developmental context could alter the course of the development of ASD symptoms.