背景:神经性贪食症(BN)是一种饮食失调,其特征是反复暴饮暴食和代偿行为。丘脑在与饮食行为相关的神经回路中起着至关重要的作用,需要在BN中进一步探索。
方法:在本研究中,招募49名BN患者和44名健康对照(HCs)。我们应用低频波动的分数幅度来研究丘脑中的区域大脑活动和功能连接(FC),以检查两组中丘脑亚区域与其他大脑区域之间的活动同步。所有结果均进行了错误发现率(p<0.05,FDR校正)校正。进行Pearson相关分析以评估患者异常临床表现与丘脑改变之间的关系(p<0.05,FDR校正)。
结果:我们发现16个丘脑亚区的BN患者和HC之间的神经活动没有显着差异。然而,与HC相比,具有BN的个体在丘脑亚区域和几个区域之间显示出减少的FC,包括双侧前额叶皮层,右下顶叶小叶,右侧辅助电机区域,右岛,扣带回和疣。此外,BN患者显示丘脑亚区和视觉关联区之间的FC增加,初级感觉运动皮层,离开小脑.在BN组中,丘脑中这些改变的FC模式与临床变量(每周暴食/清除的频率和外部饮食行为量表评分)相关。所有结果均通过FDR校正。
结论:我们的研究提供了证据,表明BN患者在静息状态下,丘脑亚区和其他脑区之间的FC被破坏。这些区域主要位于额顶叶网络内,默认模式网络,体感,视觉网络。这些发现阐明了BN的神经活动特征,并表明丘脑亚区域有可能作为未来神经调节干预的目标。
神经性贪食症(BN)的高复发率提出了临床挑战,因此,改善脑功能异常的表征和鉴定作为新疗法的直接靶标至关重要。为了研究与BN相关的神经回路,丘脑是一个关键节点,因为它是皮质-丘脑-皮质信息通路中的高阶中继点。我们的发现表明,丘脑核和其他大脑区域之间的功能连接(FC)在整个大脑中都很明显。特别是在额顶顶网络中,默认模式网络,体感,视觉网络。FC的这些变化与BN患者的饮食紊乱行为和疾病严重程度显着相关。因此,这些发现有助于确定饮食紊乱行为和BN严重程度的神经机制,并为未来的神经调节干预提供潜在目标。
BACKGROUND: Bulimia nervosa (BN) is an eating disorder characterized by recurrent binge eating and compensatory behaviors. The thalamus plays a crucial role in the neural circuitry related to eating behavior and needs to be further explored in BN.
METHODS: In this study, 49 BN patients and 44 healthy controls (HCs) were recruited. We applied the fractional amplitude of low-frequency fluctuation to investigate regional brain activity in the thalamus and functional connectivity (FC) to examine the synchronization of activity between thalamic subregions and other brain regions in both groups. All results underwent false discovery rate (p < 0.05, FDR correction) correction. Pearson correlation analysis was performed to assess the relationship between the patients\' abnormal clinical performance and the thalamic alterations (p < 0.05, FDR correction).
RESULTS: We found no significant differences in neural activity between BN patients and HCs in the sixteen thalamic subregions. However, compared to the HCs, the individuals with BN showed decreased FC between the thalamic subregions and several regions, including the bilateral prefrontal cortex, right inferior parietal lobule, right supplementary motor area, right insula, cingulate gyrus and vermis. Additionally, BN patients showed increased FC between the thalamic subregions and visual association regions, primary sensorimotor cortex, and left cerebellum. These altered FC patterns in the thalamus were found to be correlated with clinical variables (the frequency of binge eating/purging per week and external eating behavior scale scores) in the BN group. All results have passed FDR correction.
CONCLUSIONS: Our study provides evidence that there is disrupted FC between thalamic subregions and other brain regions in BN patients during resting state. These regions are primarily located within the frontoparietal network, default mode network, somatosensory, and visual network. These findings elucidate the neural activity characteristics underlying BN and suggest that thalamic subregions have potential as targets for future neuromodulation interventions.
The high recurrence rate of bulimia nervosa (BN) poses a clinical challenge, and thus, it is crucial to improve the characterization and identification of brain functional abnormalities as direct targets for novel therapies. To investigate the neural circuitry associated with BN, the thalamus is a critical node since it serves as a higher-order relay point in the cortico-thalamo-cortical information pathway. Our findings reveal that altered functional connectivity (FC) between thalamic nuclei and other brain regions is evident throughout the whole brain, particularly within the frontoparietal network, default mode network, somatosensory, and visual network. These changes in FC are significantly associated with disordered eating behavior and the severity of illness in BN patients. Therefore, these findings help identify the neural mechanisms underlying disordered eating behavior and BN severity and suggest potential targets for future neuromodulation interventions.