本研究透過功能性磁振造影 (functional Magnetic Resonance Imaging, fMRI) 探討強迫性購買者 (Compulsive Buyers, CB) 與非強迫性購買者 (Non-Compulsive Buyers, NCB) 在購物衝動與渴望情境下的神經機制差異。研究採用「渴望任務」和「購物決策任務」進行實驗，發現CB組不僅購買數量顯著更高，亦更容易被激發高渴望。同時， CB組的背外側前額葉皮質 (Dorsolateral Prefrontal Cortex, dlPFC) 活化程度顯著低於NCB組，暗示其執行控制網路 (Executive Control Network, ECN) 可能出現缺陷 (Osaka et al., 2004；Friedman et al., 2022)。動態因果建模 (Dynamic Causal Modeling, DCM) 進一步揭示，CB組在購買時，前扣帶皮層 (Anterior Cingulate Cortex, ACC) 向 dlPFC 傳遞的「衝突監控訊號」顯著減弱 (Botvinick et al., 2001)，導致其難以調整過度購買的行為。此外，心理生理交互作用分析 (Psychophysiological interaction, PPI) 證實，CB組的 dlPFC 與廣泛的抑制及自我參照網路之間存在功能性斷連。綜合以上，本研究支持CB在渴望及購物上的失控，並進一步指出行為上的失控不僅是單一腦區的異常，更可能是源自於整體神經網路之間的訊息斷連。

This study investigated the differential neural mechanisms underlying shopping impulsivity and craving between Compulsive Buyers (CB) and Non-Compulsive Buyers (NCB) using functional Magnetic Resonance Imaging (fMRI). The experimental paradigm incorporated a "craving task" and a "shopping decision task." Findings revealed that the CB group exhibited a significantly higher purchase quantity and greater ease of generating high craving levels. Furthermore, the CB group showed significantly lower activation in the Dorsolateral Prefrontal Cortex (dlPFC) compared to the NCB group, suggesting a potential impairment in the Executive Control Network (ECN) (Osaka et al., 2004; Friedman et al., 2022). Dynamic Causal Modeling (DCM) analysis further demonstrated that the "conflict monitoring signal" transmitted from the Anterior Cingulate Cortex (ACC) to the dlPFC during purchasing was significantly attenuated in the CB group (Botvinick et al., 2001), contributing to their difficulty in regulating excessive buying behavior. Additionally, Psychophysiological Interaction (PPI) analysis confirmed a functional disconnect between the dlPFC and widespread inhibitory and self-referential networks in the CB group. Collectively, these findings support the notion of compromised control over craving and shopping in CB, suggesting that behavioral dyscontrol may not stem solely from the abnormality of a single brain region but rather from disrupted connectivity across integral neural networks.

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