In the response inhibition and impulse control domain, using the stop signal task, lamotrigine increased the medial prefrontal cortex (MPFC), pregenual, subgenual, and posterior cingulate activity (PCC) in PBD over 14 weeks, while striatal activity was increased in HC. Lamotrigine’s glutametergic attenuating action is associated with reduction in bipolar depression, where MPFC, DLPFC, striatum, and PCC showed increased activation from the baseline (Chang et al, 2008). Another double-blind randomized trial using independent-component analysis, compared the change in connectivity of brain circuits with DVPX vs risperidone in PBD and HC. Here, DVPX increased the connectivity of the subgenual cortex within the affective evaluation and inhibition circuitry during response inhibition. This is similar to the earlier outcome with lamotrigine, confirming the role of subgenual cortex during impulse control with an antiepileptic agent. However, antipsychotic risperidone is associated with increased engagement of insula relative to DVPX group or HC.

At the interface of working memory and affective processing domains, using the N-Back working memory task, relative to HC, patients with PBD showed increased activation response in subgenual cingulate and ventral striatum when risperidone was administered. The VLPFC–MPFC and medial temporal regions showed greater activity with lamotrigine as well as DVPX (the two antiepileptic agents) relative to baseline while patients were remembering angry faces.

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