Hepatic encephalopathy (HE), the neuropsychiatric presentation of liverdisease, is associated with high morbidity and mortality. Reduction ofplasma ammonia remains the central therapeutic strategy. Minimal hepatic encephalopathy (MHE) is a neurocognitive disorder that affectsup to 80% of cirrhotic patients. Similar to overt hepatic encephalopathy,ammonia and oxidative stress play key roles in the pathogenesis of MHE. However, MHE is characterized by subtle deficits and psychomotorabnormalities that can only be elicited by specialized psychometric tests.