轻微型肝性脑病患者静息态下双侧楔前叶与全脑其他区域功能连接变化

目的 观察轻微型肝性脑病（MHE）患者静息态下双侧楔前叶与全脑其他区域功能连接（FC）变化。方法 对22例肝硬化伴MHE患者（MHE组）、23例肝硬化无MHE患者（NMHE组）和24名健康志愿者（对照组）行静息态fMRI，选择双侧楔前叶为种子点，采用种子体素相关性脑功能网络分析方法计算并比较各组间双侧楔前叶与全脑其他区域的FC。结果 与对照组比较，MHE组左侧楔前叶与右侧额上回、左侧中扣带回的FC及右侧楔前叶与右侧颞极、左侧颞上回、双侧前额叶和内侧扣带回的FC降低，NMHE组左侧楔前叶与右侧额中回的FC及右侧楔前叶与左侧楔前叶、左侧中扣带回的FC降低（P均<0.05）；与NMHE组比校，MHE组左侧楔前叶与右侧额上回的FC及右侧楔前叶与右侧脑岛、右侧额中/上回的FC降低（P均<0.05）。结论 MHE患者静息态下双侧楔前叶与全脑多个脑区FC存在异常，这可能是其大脑内源性神经功能损伤的机制之一。

Resting-state functional connectivity of bilateral precuneus and other brain regions in minimal hepatic encephalopathy

Objective To explore the changes of resting-state functional connectivity (FC) of bilateral precuneus and other brain regions in patients with minimal hepatic encephalopathy (MHE). Methods Twenty-two liver cirrhosis patients with MHE (MHE group), 23 liver cirrhotic patients without MHE (NMHE group) and 24 healthy subjects (control group) underwent resting-state functional MRI (rs-fMRI). Bilateral precuneus was picked as seeds, and then FC of bilateral precuneus and other brain regions were calculated for statistical analysis by using standard seed-based whole-brain correlation method. Results Compared with control group, the left precuneus showed reduced FC with the right superior frontal gyrus, left middle cingulate gyrus, while the right precuneus showed reduced FC with the right temporal pole, left superior temporal gyrus, bilateral frontal lobe and medial cingulum cortex in MHE group, and the left precuneus showed reduced FC with the right middle frontal gyrus, while the right precuneus showed reduced FC with the left precuneus and left middle cingulate gyrus in NMHE group (all P<0.05). Compared with the NMHE group, the left precuneus showed reduced FC with the right superior frontal gyrus, while the right precuneus showed reduced FC with the right insula and right superior/middle frontal gyrus in MHE group (all P<0.05). Conclusion Abnormal resting-state FC of bilateral precuneus and multiple brain regions are demonstrated in patients with MHE, which may be the mechanism of endogenous neurological impairment of MHE.