Structural and functional neural correlates of sensorimotor deficits in progression of hepatic encephalopathy

Hepatic encephalopathy (HE) is a neurological condition that occurs as a complication of liver dysfunction that involves sensorimotor symptoms in addition to cognitive and behavioral changes, particularly in cases of severe liver disease or cirrhosis. Previous studies have reported spatially distributed structural and functional abnormalities related to HE, but the exact relationship between the structural and functional alterations with respect to disease progression remains unclear. In this study, we performed surface-based cortical thickness comparisons and functional connectivity (FC) analyses between three cross-sectional groups: healthy controls (HC, <i>N</i> = 51), patients with minimal hepatic encephalopathy (MHE, <i>N</i> = 50), patients with overt hepatic encephalopathy (OHE, <i>N</i> = 51). In addition to the distributed cortical thinning that is extensively thought to be associated with cognitive decline in HE, we found significant cortical thickening in the left parahippocampal gyrus cortex in the OHE group (<i>p</i> < 0.001, <i>p</i> = 0.009) as compared to the HC and MHE group respectively, which is further corroborated by the significant correlation between the cortical thickness and digit symbol test (DST) scores. Furthermore, the decreased FC between the right postcentral gyrus and several sensory regions (bilateral somatosensory and visual cortices) was found to be significant in MHE patients as compared to the HC group. Our results revealed cross-sectional structural and functional variations concerning disease progression across different subsystems (e.g., visual, motor and sensory), providing evidence that can potentially explain the mechanisms underlying the sensorimotor and cognitive deficits related to HE.