檳榔即時效果：靜息態功能性磁振造影的功能性連結分析

研究目的：過去研究證實檳榔嚼食者可能對檳榔產生成癮。而探討檳榔即時效果可一探檳榔嚼後的正向體驗，而此將與成癮發展歷程：沉醉與濫用相關。目前嚼食檳榔在大腦的即時效果僅有湖南學者以當地嚼食習慣（檳榔蜜餞）進行研究，仍未有以台灣本地嚼食習慣的研究。本研究將以台灣嚼食習慣（包葉仔）探討嚼食檳榔對大腦功能性連結（functional connectivity ；FC）的即時效果。方法：納入檳榔成癮組 14 名、菸酒使用組 19 名，以及健康控制組 20 名，所有參與者皆為成人男性，於嚼檳前後各掃描一組靜息態功能性磁振造影，採用CONN toolbox v.22.a 與 SPM12，進行基於 21 個感興趣區的功能性連結分析，並透過檳榔成癮組和健康控制組的簡單主要嚼食效果分析，獲得從未嚼食者與檳榔成癮者的嚼檳即時效果。結果：（1）無論是檳榔成癮者或是從未嚼食者，皆在嚼檳後即時地提升 SN—MCL 的功能連結，且都有涉及大量的視覺腦區（如：lateral occipital cortex）與其他網絡之功能連結的提升。（2）從未嚼食者在嚼檳後即時地減少 ECN 內部網絡的功能連結，以及 SN—ECN、ECN—MCL、DMN—MCL 的功能連結。結論：嚼檳可能會啟動多巴胺酬賞系統，如：檳榔成癮者與從未嚼食者嚼後會即時地提升 SN 與 MCL 系統功能連結。而從未嚼食者嚼檳後即時地減少 ECN內部網絡，以及 ECN—MCL、SN—ECN 之功能連結，與抑制控制能力、執行功能、嚼檳行為控制受損有關。此外，amygdala 與後半部 DMN 的功能連結在嚼檳後即時地減少則可能代表負向感受減緩。最後，檳榔成癮者與從未嚼食者的視覺腦區與其他大腦網絡的功能連結在嚼後顯著提升，與大腦發展對成癮物質的誘因顯著性有關。

Purpose: The studies related to the acute effects of BQ are mostly from Hunan, where the locals' chewing habit is different from Taiwan(pau-hioh). This study intends to explore the acute effects of chewing betel quid on the brain's functional connectivity (FC), focusing on Taiwan's chewing habits (pau-hioh). MATERIALS AND METHODS: 14 betel-quid-dependent chewers (BQD), 19 tobacco and alcohol controls (TA), and 20 healthy controls (HC) were included in our study. All participants are adult males. Resting-state functional magnetic resonance imaging (fMRI) was performed on all participants before and after betel quid chewing. Roi-to-Roi and Seed-to-Voxel FC analyses are performed with CONN toolbox v.22.a, focusing on 4 brain networks (21 regions of interest): Executive Control network (ECN), Salience network (SN), Default mode network (DMN), Mesocorticolimbic system (MCL). The Simple main chewing effect is analyzed in the BQD and HC groups, respectively. Results: (1) The acute effect of BQ was increased FCs between SN and MCL in both BQD and HC. Moreover, the functional connectivity between visual areas and other brain networks is increased after chewing in BQD and HC; (2) In HC, the effect of chewing was decreased FCs within ECN, and decreased FCs of SN —ECN, ECN—MCL, DMN—MCL. Conclusion: Chewing BQ may activate the mesocorticolimbic dopamine pathway, which is relevant to the enhanced FCs of SN—MCL. Additionally, the acute chewing effect of suppressed FCs within ECN, between MCL and ECN, and between SN and ECN indicates disrupted executive control (e.g. inhibition function), and impaired control of drug use. Also, group HC showed weakened FCs between the amygdala and posterior DMN, suggesting less self-referential processing of thoughts and the cause of positive feelings. Finally, the enhanced FCs between visual areas and other brain networks may related to the development of incentive salience.