Contribution of neuroimaging to the understanding of social cognition in epilepsy.

Abstract

This narrative review aims to identify and summarize existing research to better understand the pathophysiological and neuroanatomical bases of social cognition deficits in people with epilepsy. The neuroanatomical basis of social cognition was primarily examined in healthy subjects. In healthy individuals, social cognition is supported by a complex network of interconnected brain regions. Facial emotion recognition relies on a distributed set of structures, including the occipitotemporal neocortex, the temporoparietal and prefrontal areas, and the putamen with a pivotal role of the amygdala. Theory of mind primarily involves the dorsal medial prefrontal cortex and temporoparietal junction, while empathy engages the anterior insular and cingulate cortices. In people with epilepsy, most functional neuroimaging studies have focused on facial emotion recognition, primarily in patients with temporal lobe epilepsy. Nevertheless, across various domains of social cognition, abnormal activations and disrupted connectivity within social cognition networks are consistently observed, regardless of the focus location. Aberrant connectivity has also been noted in the few studies involving patients with generalized epilepsy. In focal epilepsy, the amygdala remains a central region for facial emotion recognition, irrespective of whether the epilepsy is localized to the temporal or frontal lobes. For theory of mind studies, regions typically identified in healthy individuals, such as the medial prefrontal cortex, exhibit either hyperactivation or reduced activation in people with focal epilepsy, complicating interpretation. In the domain of empathy, a study involving patients with idiopathic generalized epilepsy reported decreased activation in core regions commonly identified in healthy individuals, particularly the anterior cingulate cortex and anterior insula. The limited data available in the literature suggest that key regions shared between social cognition and epilepsy networks consistently contribute to these disruptions and may serve as potential targets for future neuromodulation interventions.