Abstract
Individuals with autism spectrum disorder (ASD) show deficits in social and communicative skills, including imitation, empathy, and shared attention, as well as restricted interests and repetitive patterns of behaviors. Evidence for and against the idea that dysfunctions in the mirror neuron system are involved in imitation and could be one underlying cause for ASD is discussed in this review. Neurofeedback interventions have reduced symptoms in children with ASD by self-regulation of brain rhythms. However, cortical deficiencies are not the only cause of these symptoms. Peripheral physiological activity, such as the heart rate and its variability, is closely linked to neurophysiological signals and associated with social engagement. Therefore, a combined approach targeting the interplay between brain, body, and behavior could be more effective. Brain–computer interface applications for combined neurofeedback and biofeedback treatment for children with ASD are currently nonexistent. To facilitate their use, we have designed an innovative game that includes social interactions and provides neural- and body-based feedback that corresponds directly to the underlying significance of the trained signals as well as to the behavior that is reinforced.
Highlights
NEUROETIOLOGY OF AUTISM SPECTRUM DISORDER (ASD) Autism spectrum disorder (ASD) is an increasingly prevalent condition in the U.S with core deficits in the unique domain of human social behaviors (American Psychiatric Association, 2000; Hansen et al, 2008; Rice, 2011)
Exploring the neuroetiology of this disorder is a focus of our research which was prompted by the discovery of mirror neurons. The discovery of these visuomotor cells in monkey prefrontal cortex and the description of a similar network of areas in the human brain, or mirror neuron system (MNS, Figure 1; Rizzolatti and Craighero, 2004), has provided a testable neurobiological substrate for understanding many key concepts in human social and emotional cognition directly relevant to the behavioral and cognitive deficits observed in children with autism spectrum disorder (ASD) (Williams et al, 2001)
For example, is that dyspraxia rather than the MNS could account for imitation deficits in children with ASD (Mostofsky et al, 2006; Stieglitz Ham et al, 2011)
Summary
NEUROETIOLOGY OF AUTISM SPECTRUM DISORDER (ASD) Autism spectrum disorder (ASD) is an increasingly prevalent condition in the U.S with core deficits in the unique domain of human social behaviors (American Psychiatric Association, 2000; Hansen et al, 2008; Rice, 2011). Individuals with high functioning ASD show deficits primarily in social and communicative skills such as imitation, empathy, and shared attention, as well as restricted interests and repetitive patterns of behaviors. To bring some level of reconciliation along various observations, several investigators have proposed a compromise solution that focuses on both local overconnectivity and long range underconnectivity (Anderson et al, 2011) This is not inconsistent with the MNS hypothesis since over- and under connectivity likely characterizes this specific network. Functional, and electrophysiological evidence, we hypothesize that a range of over- and underconnectivity in children with ASD, in the MNS system, correlates with levels of performance in cognitive, emotional, and behavioral outcomes
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