To assess neuronal mechanisms of potential importance in the pathogenesis of
hepatic encephalopathy, visual evoked potentials were recorded in rabbits with acute hyperammonemic
encephalopathy, postictal
coma, and toxin-induced
coma resulting from the administration of a combination of subcoma doses of three
neurotoxins:
ammonia,
dimethyldisulfide, and
octanoic acid. The patterns of visual evoked potentials in these three syndromes were compared with those of rabbits with
hepatic encephalopathy due to
galactosamine-induced
fulminant hepatic failure. In the absence of
seizures, the patterns of visual evoked potentials associated with hyperammonemic
encephalopathy and toxin-induced
coma were fundamentally different from those associated with any stage of
hepatic encephalopathy due to
galactosamine-induced
fulminant hepatic failure. In contrast, the pattern of visual evoked potentials in early postictal
coma induced by four different precipitating factors (including toxin-induced
seizures) resembled that of late-stage
hepatic encephalopathy due to
galactosamine-induced
fulminant hepatic failure. These findings suggest that the recording of visual evoked potentials may be of value in experimentally testing hypotheses of the pathogenesis of
hepatic encephalopathy due to
fulminant hepatic failure. They indicate that acute
hyperammonemia is not a satisfactory model of
hepatic encephalopathy due to
galactosamine-induced
fulminant hepatic failure, that the occurrence of
seizures may lead to incorrect interpretation of experimental data from models of
hepatic encephalopathy, and that the syndromes of
hepatic encephalopathy due to
galactosamine-induced
fulminant hepatic failure and postictal
coma may share similar neural mechanisms. Finally, the results of this study do not support the hypothesis that
hepatic encephalopathy due to
galactosamine-induced
fulminant hepatic failure is mediated by the synergistic interaction of
ammonia,
mercaptans, and
fatty acids on the brain.