Understanding the brain mechanisms of heroin dependence is invaluable for developing effective treatment. Measurement of regional cerebral blood flow (CBF) provides a method to visualize brain circuits that are functionally impaired by heroin dependence. This study examined regional CBF alterations and their clinical associations in unmedicated heroin-dependent individuals (HDIs) using a relatively large sample. Sixty-eight (42 males, 26 females; age: 40.9 ± 7.3 years) HDIs and forty-seven (34 males, 13 females; age: 39.3 ± 9.2 years) matched healthy controls (HCs) underwent high-resolution T1 and whole-brain arterial spin labeling (ASL) perfusion magnetic resonance imaging (MRI) scans. Additionally, clinical characteristics were collected for neurocognitive assessments. HDIs showed worse neuropsychological performance than HCs and had decreased relative CBF (rCBF) in the bilateral middle frontal gyrus (MFG), inferior temporal gyrus, precuneus, posterior cerebellar lobe, cerebellar vermis, and the midbrain adjacent to the ventral tegmental area; right posterior cingulate gyrus, thalamus, and calcarine. rCBF in the bilateral MFG was negatively correlated with Trail Making Test time in HDIs. HDIs had limbic, frontal, and parietal hypoperfusion areas. Low CBF in the MFG indicated cognitive impairment in HDIs. Together, these findings suggest the MFG as a critical region in HDIs and suggest ASL-derived CBF as a potential marker for use in heroin addiction studies.

Internet gaming disorder (IGD) is becoming a matter of concern around the world. However, the neural mechanism underlying IGD remains unclear. The purpose of this paper is to explore the differences between the neuronal network of IGD participants and that of recreational Internet game users (RGU).
Imaging and behavioral data were collected from 18 IGD participants and 20 RGU under a probability discounting task. The independent component analysis (ICA) and graph theoretical analysis (GTA) were used to analyze the data.
Behavioral results showed the IGD participants, compared to RGU, prefer risky options to the fixed ones and spent less time in making risky decisions. In imaging results, the ICA analysis revealed that the IGD participants showed stronger functional connectivity (FC) in reward circuits and executive control network, as well as lower FC in anterior salience network (ASN) than RGU; for the GTA results, the IGD participants showed impaired FC in reward circuits and ASN when compared with RGU.
These results suggest that IGD participants were more sensitive to rewards, and they were more impulsive in decision-making as they could not control their impulsivity effectively. This might explain why IGD participants cannot stop their gaming behaviors even when facing severe negative consequences.

Neuroimaging studies have demonstrated that major depressive disorder (MDD) patients show blunted activity responses to reward-related tasks. However, whether abnormal reward circuits affect cognition and depression in MDD patients remains unclear. Seventy-five drug-naive MDD patients and 42 cognitively normal (CN) subjects underwent a resting-state functional magnetic resonance imaging scan. The bilateral nucleus accumbens (NAc) were selected as seeds to construct reward circuits across all subjects. A multivariate linear regression analysis was employed to investigate the neural substrates of cognitive function and depression severity on the reward circuits in MDD patients. The common pathway underlying cognitive deficits and depression was identified with conjunction analysis. Compared with CN subjects, MDD patients showed decreased reward network connectivity that was primarily located in the prefrontal-striatal regions. Importantly, distinct and common neural pathways underlying cognition and depression were identified, implying the independent and synergistic effects of cognitive deficits and depression severity on reward circuits. This study demonstrated that disrupted topological organization within reward circuits was significantly associated with cognitive deficits and depression severity in MDD patients. These findings suggest that in addition to antidepressant treatment, normalized reward circuits should be a focus and a target for improving depression and cognitive deficits in MDD patients.

Altered reward processing and cognitive deficits are often observed in patients with obsessive-compulsive disorder (OCD); however, whether the imbalance in activity between reward circuits and the cognitive control (CC) system is associated with compulsive behavior remains unknown. Sixty-eight OCD patients and 33 cognitively normal (CN) healthy subjects participated in this resting-state functional magnetic resonance imaging study. Alterations in the functional connectivity between reward circuits and the CC system were quantitatively assessed and compared between the groups. A Granger causality analysis was used to determine the causal informational influence between and within reward circuits and the CC system across all subjects. OCD patients showed a dichotomous pattern of enhanced functional coupling in their reward circuits and a weakened functional coupling in their CC system when compared to CN subjects. Neural correlates of compulsive behavior were primarily located in the reward circuits and CC system in OCD patients. Importantly, the CC system exerted a reduced interregional causal influence over the reward system in OCD patients relative to its effect in CN subjects. The limitations of this study are that it was a cross-sectional study and the potential effects of environmental and genetic factors were not explored. OCD patients showed an imbalance in the functional link between reward circuits and the CC system at rest. This bias toward a loss of control may define a pathological state in which subjects are more vulnerable to engaging in compulsive behaviors.