The Role of Temporoparietal Junction in Intentional Causal Attribution in Autism

Background: Attribution of intentions to others, a key element of what is referred to as theory-of-mind, is perhaps one of the most complex forms of human reasoning. Mental state attribution involves the interplay of a set of subprocesses, such as representation of reality, understanding one’s own beliefs and the beliefs of others, and taking others’ perspective. Understanding the cause and effect of actions is one of the skills that children learn during development. However, individuals with autism are known to have major impairments in the development of intentional causality (Baron-Cohen, 1995; Baron-Cohen et al., 1985; 1993) whilst having relatively normal or even superior development in their understanding of physical causality (Baron-Cohen, 1997; Frith, 1989; Jolliffe & Baron-Cohen, 1997). The current study investigated this dichotomy in understanding causality and its neural underpinnings in autism.

Objectives: The primary aim of this study was to examine the cognitive and neural mechanisms underlying the attribution of causal explanations to the actions of social and physical agents in individuals with autism.

Methods: Eight high-functioning adolescents and adults with autism and ten age-and-IQ-matched neurotypical controls participated in this fMRI study (data collection in progress). Non-verbal comic strip vignettes involving physical and intentional causal scenarios were presented randomly and the participants had to choose the most logical ending to each vignette. The participants indicated their response by choosing alternatives A, B or C with a button press. The data acquired from a Siemens 3T Allegra scanner were analyzed using Statistical Parametric Mapping (SPM2).

Results: During intentional causal attribution, the performance of participants with autism was significantly poorer with longer response times relative to controls. However, no reliable group difference was found in performance or response time in the physical causality condition. At the cortical level, the underactivation in autism was most pronounced in right superior temporal sulcus at the temporoparietal junction (TPJ), an area associated with theory-of-mind. In addition, the participants with autism also showed reliably lower activation in right inferior parietal lobule, left orbitofrontal cortex and left precuneus. However, no group difference in activation was found in the medial prefrontal cortex (MPFC) while attributing intentional causality.

Conclusions: The findings of this study underscore the impairments in social cognition and theory-of-mind in people with autism, in particular their difficulty in attributing intentions to social agents. Since we did not find any group difference in activation in MPFC in this study, the findings re-ignite the debate about the relative role of temporoparietal junction and medial prefrontal cortex in theory-of-mind. It is possible that the TPJ might be playing a critical role in reasoning about the representational mental states of the character (Saxe and Kanwisher, 2003; Saxe et al., 2006). Functional and effective connectivity analyses are in progress, the results of which might provide more information on the communication between MPFC and TPJ and also the relative functions of each of these regions.