Aberrant causal inference and presence of a compensatory mechanism in autism spectrum disorder

Autism spectrum disorder (ASD) is characterized by a panoply of social, communicative, and sensory anomalies. As such, a central goal of computational psychiatry is to ascribe the heterogenous phenotypes observed in ASD to a limited set of canonical computations that may have gone awry in the disorder. Here, we posit causal inference - the process of inferring a causal structure linking sensory signals to hidden world causes - as one such computation. We show that audio-visual integration is intact in ASD and in line with optimal models of cue combination, yet multisensory behavior is anomalous in ASD because this group operates under an internal model favoring integration (vs. segregation). Paradoxically, during explicit reports of common cause across spatial or temporal disparities, individuals with ASD were less and not more likely to report common cause, particularly at small cue disparities. Formal model fitting revealed differences in both the prior probability for common cause (p-common) and choice biases, which are dissociable in implicit but not explicit causal inference tasks. Together, this pattern of results suggests (i) different internal models in attributing world causes to sensory signals in ASD relative to neurotypical individuals given identical sensory cues, and (ii) the presence of an explicit compensatory mechanism in ASD, with these individuals putatively having learned to compensate for their bias to integrate in explicit reports.

Automated summary

Autism spectrum disorder (ASD) is a disorder characterized by social, communicative, and sensory anomalies. Computational psychiatry aims to understand the underlying computations that give rise to the heterogeneous phenotypes observed in ASD. This study suggests that individuals with ASD have different internal models for attributing world causes to sensory signals compared to neurotypical individuals, and that there may be an explicit compensatory mechanism in ASD to counterbalance their bias towards integration.