ventral tegmental area to the NACC, hippocampus, and medial frontal cortex compared to the control group. Previous studies have initially explored the causal brain mechanism in the resting state of substance use disorder; however, due to limitations such as small sample size and lack of independent verification, further follow-up studies are required to investigate the causal brain mechanism in the resting state of substance use disorder more comprehensively. In this study, we employed MVPA and spectral DCM to investigate the underlying causal brain mechanisms during rest in a relatively large sample of patients diagnosed with AUD. We have also observed that individuals with AUDs exhibit atypical EC from the cortex to reward-related brain regions, which may represent a shared underlying neural mechanism for substance use disorders. Furthermore, we conducted independent validation of our findings, thereby offering valuable insights for studying the causal brain mechanisms associated with substance use disorders.
