Theory of mind deficits in children with congenital heart disease

The cognitive and academic challenges faced by children with congenital heart disease (CHD) as they grow older have been extensively researched. Fewer studies have focused on characterizing the nature and severity of the psychosocial challenges, despite their potential importance for the children’s quality of life. I recently speculated that deficits in social cognition and, in particular, theory of mind are among the morbidities of children with CHD. This speculation was based primarily on the moderately severe and persistent pragmatic language deficits (e.g. storytelling, pretend play) of a group of children with d-transposition of the great arteries (d-TGA). Such deficits, which are usually discussed in the context of autism spectrum disorders, impair a child’s ability to process social information and to read other people and discern their inner states, threatening success in establishing and sustaining social relationships. Calderon et al. provide the first direct evidence to support aspects of this conjecture, showing that children with d-TGA were less accurate than typically developing children in analysing false belief stories, suggesting a reduced capacity to put themselves ‘in the shoes’ of story characters in order to predict their behavior. This study is an important initial step in evaluating the broad domain of social cognition in children with CHD. It is a multifaceted concept, providing many avenues for future research. Do children with CHD have greater difficulty than their typically developing peers in discerning internal states on the basis of facial expression, nonverbal cues, or paralinguistic cues such as prosody? Do they have greater difficulty understanding jokes, sarcasm, irony, and other messages in which the literal interpretation conflcts with the intended interpretation? Do they have difficulty identifying and communicating their own emotions, as well as those of other people (i.e. alexithymia)? In terms of prevention and remediation, it will be important in future research to address several potential explanations for an increased risk of social cognition deficits in children with CHD. First, the embryological event that resulted in CHD might also affect the brain structures or circuits responsible for the processing of social and affective information. Children with CHD have concomitant brain abnormalities, particularly disorders of white matter, even before undergoing reparative interventions. It is noteworthy that other groups of children with such disorders (e.g. extremely low birthweight or preterm children) also tend to exhibit behaviors associated with autism spectrum disorders. Second, the social cognition deficits might be the result of interventions undertaken to correct or palliate CHD. This possibility seems unlikely, however, as such interventions tend to explain little of the variability in the cognitive outcomes of children with CHD. Third, the social cognition deficits might be secondary to the neuropsychological deficits associated with CHD. Among the areas in which deficits are commonly reported are visualspatial skills, attention, and executive function. Indeed, in the Calderon et al. study, children who performed poorly on the false belief stories also showed executive function deficits, specifically in self-regulation and inhibiting interference. Such co-occurrence in a cross-sectional study does not necessarily indicate mediation, but it is consistent with this hypothesis. Social cognition deficits are frequently observed in children with other neurodevelopmental disorders. For example, on a group basis, children with specific learning disabilities, traumatic brain injuries, and attention-deficit–hyperactivity dis-