Abstract
There is increasing evidence that cirrhosis may affect functional connectivity among various brain regions in patients prior to onset of overt hepatic encephalopathy (HE). However, most investigators have focused mainly on alterations in functional connectivity strengths, and the changes in functional connectivity density (FCD) are largely unknown. Here, we investigated alterations in resting-state FCD in patients with hepatitis B virus-related cirrhosis (HBV-RC) without overt HE. Totally, 31 patients with HBV-RC without overt HE and 30 age- and sex-matched healthy controls underwent resting-state functional MRI examinations. FCD mapping was employed to compute local and global FCD maps. Then, short-range and long-range FCD values were calculated and voxel-based comparisons were performed between the two groups. The HBV-RC group showed significant decreases in FCD, including decreased short-range FCDs in the bilateral middle cingulum gyrus/precuneus, the bilateral cuneus, and the left lingual gyrus/inferior occipital gyrus and decreased long-range FCD in the bilateral cuneus/precuneus. In addition, the decreased long-range FCD in the bilateral cuneus/precuneus in the HBV-RC group was related to performance on the psychometric hepatic encephalopathy score (PHES) test. These findings suggest aberrant functional connectivity density in cirrhotic patients prior to overt HE onset, which may provide better insight into understanding the pathophysiological mechanisms underlying the cirrhotic-related cognitive impairment.
Highlights
Hepatitis B virus infection remains a serious public health problem, with more than 350 million people chronically infected worldwide [1]
About 1.0–2.4% of these patients proceed to hepatitis B virus-related cirrhosis (HBVRC) [1]
We investigate whether the cognitive abnormalities in patients with hepatitis B virus-related cirrhosis (HBV-RC) without overt Hepatic encephalopathy (HE) were related to these changes in functional connectivity density (FCD)
Summary
Hepatitis B virus infection remains a serious public health problem, with more than 350 million people chronically infected worldwide [1]. Hepatic encephalopathy (HE) is the most serious neuropsychiatric complication of end-stage HBV-RC [1, 2] They always suffer from a broad spectrum of mental disorders ranging from subtle cognitive dysfunction to stupor and coma [2]. Increasing evidence indicates that various degrees of neurocognitive deficits are common, even in patients without any signs of overt HE [3, 4]. These neurocognitive dysfunctions are increasingly relevant because they are associated with poorer quality of life [5], deterioration of daily function [6], and poor prognosis [7]. The pathophysiological mechanisms underlying these deficits are still not fully understood
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