In patients suffering from hepatic failure, the brain is subject to defined morphological and functional changes known as hepatic encephalopathia (HE). The morphological changes are dominated by glial cells (Alzheimer-type II astrocytes). It has recently been possible to demonstrate, that the retinal glia (Müller) cells undergo similar morphological changes. The present study was carried out in order to reveal if these Müller cell changes cause any characteristic functional deficits. We examined 11 patients with different stages of HE due to liver cirrhosis. Six patients were at stage 0 or 1 (group I) and five at stage 2 or 3 (group II). They underwent ophthalmological routine examination, colour vision testing and standard ERG recording. None of the patients reported impaired vision, in daylight or at night. There were no fundus abnormalities except very mild changes of the pigment epithelium and abnormal reflexes of the inner limiting membrane, especially in the higher HE stages. The number of confusions in the colour arrangement test increased with the higher stages of HE, preferably in the tritan axis. The scotopic a- and b-waves of the electroretinogram (ERG) were almost unchanged in group I and significantly decreased and delayed in group II. The photopic ERG b-wave amplitudes were changed in a similar fashion. Oscillatory potentials proved to be most sensitive to hepatotoxic changes. Their latencies were significantly delayed even in group I. Amplitudes were decreased significantly only in group II. Patients suffering from hepatic failure and accompanying HE display functional abnormalities of the retina. These are best demonstrated by the ERG, and correlate well with the degree of HE. A hypothesis is presented that relates the observed functional changes to altered neurotransmitter levels and impaired retinal glial-neuronal interaction, due to Müller cell damage caused by elevated ammonia levels.