An altered brain metabolism in the parietal and prefrontal regions of the cerebral cortex as well as cognitive alterations have been found in patients suffering from hepatic encephalopathy. The neural mechanisms underlying these metabolically induced cognitive alterations, however, are not known. Since patients with liver cirrhosis without clinically overt encephalopathy already show an impaired performance in a flicker light test, the aim of this study was to analyze the normal and pathologically impaired neural mechanisms of these patients using functional magnetic resonance imaging (fMRI). Nine subjects at the early stage of encephalopathy [nonmanifest hepatic encephalopathy (nmHE)] and ten controls underwent scanning, while they indicated the apparent transition from a steady light to the onset of a flicker light, that is, the critical flicker frequency (CFF). Judgement-related blood oxygenation level-dependent (BOLD) activation was decreased in nmHE compared to controls in the right inferior parietal cortex (IPL). Furthermore, the analysis of psychophysiologic interaction suggests impaired neural interaction in patients with nmHE, especially between the IPL and the parietooccipital cortex (Poc), the intraparietal sulcus, the anterior cingulate cortex (ACC), the right prefrontal cortex (PFC), the medial temporal lobe, and the extrastriate cortex V5. In contrast, nonmanifest patients revealed an enhanced coupling between IPL and the postcentral cortex. Our findings provide evidence of an early-impaired and compensatory neural mechanism during visual judgement already in the earliest stages of hepatic encephalopathy and suggest an aberrant coupling between cerebral regions in the dysmetabolic brain.