Abstract

Purpose Gray matter volume loss, regional cortical thinning, and local gyrification index alteration have been documented in minimal hepatic encephalopathy (MHE). Fractal dimension (FD), another morphological parameter, has been widely used to describe structural complexity alterations in neurological or psychiatric disease. Here, we conducted the first study to investigate FD alterations in MHE. Methods and Materials We performed high-resolution structural magnetic resonance imaging on cirrhotic patients with MHE (n = 20) and healthy controls (n = 21). We evaluated their cognitive performance using the psychometric hepatic encephalopathy score (PHES). The regional FD value was calculated by Computational Anatomy Toolbox (CAT12) and compared between groups. We further estimated the association between patients' cognitive performance and FD values. Results MHE patients presented significantly decreased FD values in the left precuneus, left supramarginal gyrus, right caudal anterior cingulate cortex, right isthmus cingulate cortex, right insula, bilateral pericalcarine cortex, and bilateral paracentral cortex compared to normal controls. In addition, the FD values in the right isthmus cingulate cortex and right insula were shown to be positively correlated with patients' cognitive performance. Conclusion Aberrant cortical complexity is an additional characteristic of MHE, and FD analysis may provide novel insight into the neurobiological basis of cognitive dysfunction in MHE.

Highlights

  • As a frequent neurocognitive complication of cirrhosis, hepatic encephalopathy (HE) results from the escape of substances from the liver, which can cause hyperammonemia or other metabolic disturbance [1]

  • minimal hepatic encephalopathy (MHE) patients performed worse on psychometric hepatic encephalopathy score (PHES) tests compared to healthy controls, suggesting cognitive impairment

  • The ROI-based analysis showed decreased Fractal dimension (FD) in MHE patients compared to healthy controls in the left precuneus, left paracentral gyrus, left supramarginal gyrus, and left pericalcarine cortex and in the right caudal anterior cingulate cortex, right pericalcarine cortex, right isthmus cingulate cortex, right insula cortex, and right paracentral cortex

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Summary

Introduction

As a frequent neurocognitive complication of cirrhosis, hepatic encephalopathy (HE) results from the escape of substances from the liver, which can cause hyperammonemia or other metabolic disturbance [1]. It can result in a wide variety of symptoms, from slight cognitive impairment up to coma or even death. The voxelbased morphometry (VBM) studies have indicated that cirrhotic patients with MHE have reduced gray matter volume, primarily in the middle and inferior frontal cortex, anterior cingulate cortex, putamen, paracentral lobule, and cerebellum posterior lobe [6,7,8].

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