Resting-state functional connectivity of bilateral precuneus and other brain regions in minimal hepatic encephalopathy
10.13929/j.1003-3289.201806151
- Author:
Sha LUO
1
Author Information
1. Department of Radiology, the Second Affiliated Hospital of Chongqing Medical University
- Publication Type:Journal Article
- Keywords:
Functional connectivity;
Functional magnetic resonance imaging;
Hepatic encephalopathy;
Precuneus
- From:
Chinese Journal of Medical Imaging Technology
2019;35(3):321-325
- CountryChina
- Language:Chinese
-
Abstract:
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.
