Objective:  This study was conducted to explore differences in cortical thickness between subjects with bipolar disorder and healthy comparison subjects using cortical surface‐based analysis. Methods:  Brain magnetic resonance images were acquired from 25 subjects with bipolar disorder and 21 healthy comparison subjects. Cortical surface‐based analysis was conducted using the Freesurfer application. Group differences in cortical thickness, defined by the distance from gray/white boundary to the pial surface, were assessed using statistical difference maps. Results:  Subjects with bipolar disorder exhibited significantly decreased cortical thickness in left cingulate cortex, left middle frontal cortex, left middle occipital cortex, right medial frontal cortex, right angular cortex, right fusiform cortex and bilateral postcentral cortices, relative to healthy comparison subjects (all p < 0.001). Duration of illness in bipolar subjects was inversely correlated with the cortical thickness of the left middle frontal cortex. Conclusions:  Cortical thinning was present in multiple prefrontal cortices in bipolar disorder. There was also cortical thinning in sensory and sensory association cortices, which has not been reported in previous studies using region‐of‐interest or voxel‐based morphometry methods. Cortical thinning observed in the current study may be related to impairment of emotional, cognitive, and sensory processing in bipolar disorder but longitudinal studies will be necessary to test this hypothesis.

Background and aims: The aim of the present study was to test the impulsivities and compulsivities of behavioral addictions, including Internet gaming disorder (IGD) and gambling disorder (GD), by directly comparing them with alcohol use disorder (AUD) and a healthy control (HC) group. Methods: We enrolled male patients who were diagnosed with IGD, GD or AUD, with 15 patients per group, as well as 15 HCs. Trait impulsivity was measured using the Barratt Impulsiveness Scale version 11 (BIS-11). The stop-signal test (SST) from the Cambridge Neuro-psychological Test Automated Battery (CANTAB) was used to assess the patients’ abilities to inhibit prepotent responses. Compulsivity was measured using the intra–extra dimensional set shift (IED) test from the CANTAB. The Trail Making Test (TMT) was also used in this study. Results: The IGD and AUD groups scored significantly higher on the BIS-11 as a whole than did the HC group (p = 0.001 and p = 0.001, respectively). The IGD and AUD groups also scored significantly higher on the BIS-11 as a whole than did the GD group (p = 0.006 and p = 0.001, respectively). In addition, the GD group made significantly more errors (p = 0.017 and p = 0.022, respectively) and more individuals failed to achieve criterion on the IED test compared with the IGD and HC groups (p = 0.018 and p = 0.017, respectively). Discussion: These findings may aid in the understanding of not only the differences in categorical aspects between individuals with IGD and GD but also in impulsivity–compulsivity dimensional domains. Conclusion: Additional studies are needed to elucidate the neurocognitive characteristics of behavioral addictive disorders in terms of impulsivity and compulsivity.

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BackgroundPathological gambling (PG) and obsessive-compulsive disorder (OCD) are conceptualized as a behavioral addiction, with a dependency on repetitive gambling behavior and rewarding effects following compulsive behavior, respectively. However, no neuroimaging studies to date have examined reward circuitry during the anticipation phase of reward in PG compared with in OCD while considering repetitive gambling and compulsion as addictive behaviors.Methods/Principal FindingsTo elucidate the neural activities specific to the anticipation phase of reward, we performed event-related functional magnetic resonance imaging (fMRI) in young adults with PG and compared them with those in patients with OCD and healthy controls. Fifteen male patients with PG, 13 patients with OCD, and 15 healthy controls, group-matched for age, gender, and IQ, participated in a monetary incentive delay task during fMRI scanning. Neural activation in the ventromedial caudate nucleus during anticipation of both gain and loss decreased in patients with PG compared with that in patients with OCD and healthy controls. Additionally, reduced activation in the anterior insula during anticipation of loss was observed in patients with PG compared with that in patients with OCD which was intermediate between that in OCD and healthy controls (healthy controls < PG < OCD), and a significant positive correlation between activity in the anterior insula and South Oaks Gambling Screen score was found in patients with PG.ConclusionsDecreased neural activity in the ventromedial caudate nucleus during anticipation may be a specific neurobiological feature for the pathophysiology of PG, distinguishing it from OCD and healthy controls. Correlation of anterior insular activity during loss anticipation with PG symptoms suggests that patients with PG fit the features of OCD associated with harm avoidance as PG symptoms deteriorate. Our findings have identified functional disparities and similarities between patients with PG and OCD related to the neural responses associated with reward anticipation.