Although many examples exist for shared neural representations of self and other, it is unknown how such shared representations interact with the rest of the brain. Furthermore, do high-level inference-based shared mentalizing representations interact with lower level embodied/simulation-based shared representations? We used functional neuroimaging (fMRI) and a functional connectivity approach to assess these questions during high-level inference-based mentalizing. Shared mentalizing representations in ventromedial prefrontal cortex, posterior cingulate/precuneus, and temporo-parietal junction (TPJ) all exhibited identical functional connectivity patterns during mentalizing of both self and other. Connectivity patterns were distributed across low-level embodied neural systems such as the frontal operculum/ventral premotor cortex, the anterior insula, the primary sensorimotor cortex, and the presupplementary motor area. These results demonstrate that identical neural circuits are implementing processes involved in mentalizing of both self and other and that the nature of such processes may be the integration of low-level embodied processes within higher level inference-based mentalizing.

Lesion, functional imaging, and single-unit studies in human and nonhuman animals have demonstrated a role for the amygdala in processing stimuli with emotional and social significance. We investigated the recognition of a wide variety of facial expressions, including basic emotions (e.g., happiness, anger) and social emotions (e.g., guilt, admiration, flirtatiousness). Prior findings with a standardized set of stimuli indicated that recognition of social emotions can be signaled by the eye region of the face and is disproportionately impaired in autism (Baron-Cohen, Wheelwright, & Jolliffe, 1997). To test the hypothesis that the recognition of social emotions depends on the amygdala, we administered the same stimuli to 30 subjects with unilateral amygdala damage (16 left, 14 right), 2 with bilateral amygdala damage, 47 brain-damaged controls, and 19 normal controls. Compared with controls, subjects with unilateral or bilateral amygdala damage were impaired when recognizing social emotions; moreover, they were more impaired in recognition of social emotions than in recognition of basic emotions, and, like previously described patients with autism, they were impaired also when asked to recognize social emotions from the eye region of the face alone. The findings suggest that the human amygdala is relatively specialized to process stimuli with complex social significance. The results also provide further support for the idea that some of the impairments in social cognition seen in patients with autism may result from dysfunction of the amygdala.

“Theory of mind,” the ability to make inferences about others' mental states, seems to be a modular cognitive capacity that underlies humans' ability to engage in complex social interaction. It develops in several distinct stages, which can be measured with social reasoning tests of increasing difficulty. Individuals with Asperger's syndrome, a mild form of autism, perform well on simpler theory of mind tests but show deficits on more developmentally advanced theory of mind tests. We tested patients with bilateral damage to orbito-frontal cortex ( n = 5) and unilateral damage in left dorsolateral prefrontal cortex ( n = 5) on a series of theory of mind tasks varying in difficulty. Bilateral orbito-frontal lesion patients performed similarly to individuals with Asperger's syndrome, performing well on simpler tests and showing deficits on tasks requiring more subtle social reasoning, such as the ability to recognize a faux pas. In contrast, no specific theory of mind deficits were evident in the unilateral dorsolateral frontal lesion patients. The dorsolateral lesion patients had difficulty only on versions of the tasks that placed demands on working memory.

This study tested the hypothesis that Williams syndrome, a rare genetic neurodevelopmental disorder with an unusual cognitive phenotype, involves spared abilities in the domain of understanding other minds. A group of retarded adults with Williams syndrome was compared to an age-, IQ-, and language-matched group of adults with Prader-Willi syndrome, another genetic disorder without the cognitive characteristics of Williams syndrome, and a group of age-matched normal adults, on a task that taps mentalizing ability. The task involved selecting the correct labels to match photographs of complex mental state expressions in the eye region of the face. The adults with Williams syndrome performed significantly better than the adults with Prader-Willi on this task, and about half the group performed in the same range as the normal adults. These findings are consistent with anecdotal evidence about Williams syndrome and provide evidence that mentalizing is a distinct cognitive domain. This spared cognitive capacity may be linked to the relative sparing of limbic-cerebellar neural substrate in Williams syndrome, which is also connected to cortico-frontal regions that are known to be involved in understanding complex mental states.

Two cognitive anomalies have been found in autism: a superiority on the Embedded Figures Task and a deficit in “theory of mind.” Using adult-level versions of these tasks, the present study investigated if parents of children with Asperger Syndrome might show a mild variant of these anomalies, as might be predicted from a genetic hypothesis. Significant differences were found on both measures. Parents were significantly faster than controls on the Embedded Figures Task and slightly but significantly less accurate at interpreting photographs of the eye region of the face in terms of mental states. The results are discussed in terms of the broader cognitive phenotype of Asperger Syndrome and in terms of their implications for cognitive neuroscientific theories of the condition.

Current theories of visual imagery hold that the same neural processes govern both the representation of real objects and the representation of imagined (but real) objects. Here we test whether the representation of imagined (real) objects and the representation of imagined (but unreal) objects depend on the same or different neurocognitive processes. A likely clinical group for a dissociation between these two types of imagination are children with autism, since they show deficits in imaginative play, impoverished imagination is part of their diagnosis, but they can search for hidden objects. The present study explored imagination in autism using experimental methods. Experiment 1 investigated if children with autism could introduce changes to their representations of people and houses, using Karmiloff-Smith's (1989) technique of asking children to draw “impossible” people or houses. Results showed that children with autism were significantly worse than matched controls in their ability to introduce “unreal” changes to their representations of people and houses. Instead, they tended to draw real people or objects. Experiment 2 investigated whether the performance in Experiment 1 by children with autism was due to an inability to disengage from “real world” representations, as executive dysfunction theorists would argue. To do this, the experimenter instructed them on what to draw and how to draw it. Results showed that even when executive control passed to the experimenter in this way, the children with autism were still significantly impaired in their ability to draw imaginary but unreal things relative to the matched controls. Experiment 3 investigated whether the results from Experiments 1 and 2 arose because of a generativity deficit in autism, which might be the executive dysfunction theorists' alternative account. To test this, the same subjects were given a test of Verbal Fluency and a test of imagining multiple functions of a brick. Results showed that the children with autism were no worse than clinical controls in their ability to generate ideas about real objects, suggesting that a global generativity deficit cannot explain the previous findings. Rather, these results point to a specific impairment in the ability to imagine unreal objects. This is discussed in terms of its possible neural dissociability from other kinds of imagery, and in terms of its possible relationship to theory of mind.

Many species can respond to the behavior of their conspecifics. Human children, and perhaps some nonhuman primates, also have the capacity to respond to the mental states of their conspecifics, i.e., they have a “theory of mind.” On the basis of previous research on the theory-of-mind impairment in people with autism, together with animal models of intentionality, Brothers and Ring (1992) postulated a broad cognitive module whose function is to build representations of other individuals. We evaluate the details of this hypothesis through a series of experiments on language, face processing, and theory of mind carried out with subjects with Williams syndrome, a rare genetic neurodevelopmental disorder resulting in an uneven lin-guisticocognitive profile. The results are discussed in terms of how the comparison of different phenotypes (e.g., Williams syndrome, Down syndrome, autism, and hydrocephaly with associated myelomeningocele) can contribute both to understanding the neuropsychology of social cognition and to current thinking about the purported modularity of the brain.