Abstract
The cognitive control network (CCN) is a network responsible for multiple executive functions, which are impaired in covert hepatic encephalopathy (CHE). We aimed to use functional connectivity (FC) magnetic resonance imaging to test the hypothesis that CHE manifested with disconnection within the CCN, which is associated with impaired neuropsychiatric and biochemical profiles. CHE was detected with abnormally low psychometric hepatic encephalopathy scores (PHES) (total cut-off score <−4). Two seeds in the dorsal anterior cingulate cortex (dACC) and the dorsolateral prefrontal cortex (DLPFC) were used to calculate the FC map within the CCN. Pearson correlation analysis was performed between the CCN and psychometric, biochemical profiles including ammonia, Interleukin (IL)-6, and tumor necrosis factor (TNF)-α. Eighteen CHE, 36 non-HE (NHE) cirrhotic patients and 36 controls were studied. Significant differences in FC were noted among groups, which revealed CHE patients had a lower FC in the bilateral lateral occipital cortex (seed in the bilateral dACC) and in the right lateral occipital and precuneus cortices (seed in the left DLPFC) (P < 0.05, corrected) compared with NHE. Progressively decreased FC in the left precentral gyrus within the CCN was noted from control, NHE to CHE. PHES positively and biochemistry negatively correlated with FC in the CCN. In conclusion, CHE patients showed aberrant FC within the CCN which is correlated with both cognitive dysfunction and biochemical profiles. Ammonia and pro-inflammatory cytokines may contribute to the occurrence of aberrant connectivity. Impaired FC within the CCN may serve as a complementary biomarker for CHE.
Highlights
Hepatic Encephalopathy (HE), ranging from subtle alterations to stupor and coma, is a common and serious neuropsychiatric syndrome that occurs in cirrhotic patients
We examine the hypothesis that the negativity bias among cirrhotic patients with and without covert hepatic encephalopathy (CHE) may reflect a deficit in the control of cognition, potentially associated with deficits in brain regions supporting the cognitive control network (CCN), such as dorsolateral prefrontal cortex (DLPFC) and dorsal ACC22,23
There was no significant difference in gender, age, and mood status between groups (Table 1)
Summary
Hepatic Encephalopathy (HE), ranging from subtle alterations to stupor and coma, is a common and serious neuropsychiatric syndrome that occurs in cirrhotic patients. Reduced resting-state functional connectivity with respect to attention, such as default mode network (DMN), dorsal attention network (DAN) and anterior cingulate cortex (ACC), has been associated with cognitive dysfunction in CHE compared to controls[2,3,4]. Evidence has shown that pro-inflammatory cytokines mediate the hepatic inflammation, apoptosis and necrosis of liver cells and induce cholestasis and fibrosis in patients with chronic liver diseases[19] These cytokines can act synergistically with ammonia to affect brain function in humans and animals with cirrhosis[19]. The interaction between serum markers (ammonia and pro-inflammatory cytokines) and the resting-state brain network remains unknown
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