As children develop, what changes in how they understand the behaviours of other people? Research into the development of children's 'Theory of Mind' (ToM i.e. their naïve beliefs about how other minds work and govern behaviour) has primarily focused on whether children predict others' actions considering their beliefs and goals or whether they 'egocentrically' base their predictions on their own mental states (e.g. Wellman, Cross, & Watson, 2001). In both cases, whether the goals are those of the child or of the other person, the assumption is that children predict actions will be in the service of goals-that they are part of rational plans (e.g. Baker, Saxe, & Tanenbaum, 2009; Gergely & Csibra, 2003). However, many behaviours are in fact not based on plans; human actions are routinely rooted in reflexive habits, not reflective plans (e.g.

Background Bipolar disorder (BD) is a familial psychiatric disorder associated with frontotemporal and subcortical brain abnormalities. It is unclear whether such abnormalities are present in relatives without BD, and little is known about structural brain trajectories in those at risk. Method Neuroimaging was conducted at baseline and at 2-year follow-up interval in 90 high-risk individuals with a first-degree BD relative (HR), and 56 participants with no family history of mental illness who could have non-BD diagnoses. All 146 subjects were aged 12–30 years at baseline. We examined longitudinal change in gray and white matter volume, cortical thickness, and surface area in the frontotemporal cortex and subcortical regions. Results Compared to controls, HR participants showed accelerated cortical thinning and volume reduction in right lateralised frontal regions, including the inferior frontal gyrus, lateral orbitofrontal cortex, frontal pole and rostral middle frontal gyrus. Independent of time, the HR group had greater cortical thickness in the left caudal anterior cingulate cortex, larger volume in the right medial orbitofrontal cortex and greater area of right accumbens, compared to controls. This pattern was evident even in those without the new onset of psychopathology during the inter-scan interval. Conclusions This study suggests that differences previously observed in BD are developing prior to the onset of the disorder. The pattern of pathological acceleration of cortical thinning is likely consistent with a disturbance of molecular mechanisms responsible for normal cortical thinning. We also demonstrate that neuroanatomical differences in HR individuals may be progressive in some regions and stable in others.

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