Hepatic encephalopathy (HE) is clinically characterized by a large variety of symptoms including motor symptoms, cognitive deficits, as well as changes in the level of alertness up to hepatic coma. A number of pathological processes affecting glial and neuronal function have been identified, including hyper-ammonia, changes within the excitatory and inhibitory transmitter systems, as well as osmolytic changes with consecutive cell swelling. One explanation how these pathological processes result in neurological deficits in HE is the concept of pathologically synchronized oscillations within and between relevant brain regions. A number of studies suggest that the cognitive deficits and the reduced level of alertness in patients with HE can be attributed to a significantly slowed and pathologically synchronized spontaneous oscillatory brain activity, depending on the grade of HE. Moreover, HE motor symptoms, like postural tremor called"mini asterixis," have recently been shown to be associated with abnormal thalamo-cortical and cortico-muscular synchronization. Indirect evidence exists from studies of processing and recognition of flicker stimuli that in HE slowing of oscillations also occurs in the visual system. Taken together, pathological synchronization of neuronal activity may turn out to be a promising pathophysiological concept for linking neuronal dysfunction to the diversity of clinical deficits in HE.