Cortical-structural insights into empathy and its correlates

Insights into the brain structure underlying empathy – understanding others’ mental states (cognitive empathy) and responding to them with an appropriate emotion (aff ective empathy) – are fragmented. Here, we integrate cortical-structural and purely behavioural insights into empathy and its correlates across two MRI studies of cortical thickness (CT) and surface area (SA), critical and complementary constituents of the cerebral cortex. Chapter 1 reviews the relevant literature. Chapter 2 presents a study on CT and SA in relation to empathy and empathising-systemising, and the eff ects of autism, sex, and age. Autistic adults had uniquely lower cognitive empathy and a higher “D-score” (refl ecting higher systemising than empathy); lower empathy was also observed in autistic children and adolescents. There were sex-by-diagnosis and age-by-diagnosis interactions for empathy in adults, with higher empathy in females and older adults in the non-autistic population only. In this population, higher SA (but not CT) corresponded to lower empathy and a higher D-score; the empathy relationships were observed for SA clusters underlying meta-analytic task-based activations of empathy, both cognitive and aff ective. Selectively, SA within these empathy clusters, and SA within functional networks spanning the entire cortex, interacted with autism in relation to empathy, diff ered by sex, and diff ered by age from childhood to adulthood. Chapter 3 presents a study on CT and SA in relation to empathy and psychopathy in the incarcerated male population. Factor 1 of psychopathy (Interpersonal/Aff ective) was uniquely negatively related to aff ective empathy, while Factor 2 of psychopathy (Lifestyle/Antisocial) was uniquely negatively related to cognitive empathy. Cortical structure was not related to empathy, although there was eff ect-size diff erentiation by cytoarchitectonic class and/or functional network. Conversely, cortical structure was related to psychopathy, most evidently SA to Factor 1, both in univariate inference and multivariate prediction. The high-psychopathy group had uniquely lower aff ective empathy and higher SA (but not CT); across the cortex, eff ect sizes were largest in the paralimbic class and somatomotor network, and meta-analytic task-based activations corroborated aff ective/sensory importance. Finally, the total sample revealed anterior-posterior gradients of structural covariance, which were replicated in a community sample. In the high-psychopathy group, the gradient of CT (but not SA) was globally compressed. Chapter 4 draws conclusions across the two studies. Comprehensive mapping of CT and SA suggested negative SA-empathy relationships in the general population, along with interactions for autism, and positive SA-psychopathy relationships in the incarcerated population, along with CT-covariance diff erences for psychopathy. A “mirror opposite” of empathy itself was suggested as well, with a uniquely cognitive diff erence for autism and a uniquely aff ective diff erence for psychopathy. Whilst not free from limitations, our insights aim to inform models of cortical structure and empathy, support for autistic individuals, and the treatment of psychopathic traits.