Hepatic encephalopathy (HE) is a potentially reversible, metabolically caused complication of acute or chronic liver diseases such as cirrhosis, which is characterized by neuropsychiatric abnormalities. Nearly 70% of cirrhotic patients experience mild levels of HE and approximately 30% of end-stage patients experience significant HE symptoms, many approaching coma (Mullen et al., 1999). Although the pathophysiology of HE is not yet clearly understood, the accumulation of ammonia in the brain due to the liver's inability to remove toxins (including ammonia) is thought to play a key role in the pathogenesis of HE. Other factors, which are not mutually exclusive, include increased GABA-ergic tone, selective alterations of the blood-brain barrier permeability and changes in neurotransmitter systems. The broad spectrum of symptoms in HE include forgetfulness, confusion, disorientation, concentration and memory problems, changes in mood, decreased alertness and responsiveness, changes in sleep habits, muscle tremors and stiffness, speech impairments, uncontrollable movements, agitation (Ferenci et al., 2002).