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Visual Evoked Potentials in Encephalopathy Induced by Galactosamine, Ammonia, Dimethyldisulfide, and Octanoic Acid
Author(s) -
Zeneroli Maria L.,
Ventura Ezio,
Baraldi Mario,
Penne Alessandro,
Messori Elena,
Zieve Leslie
Publication year - 2007
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840020504
Subject(s) - lethargy , coma (optics) , hepatic encephalopathy , pathogenesis , visual evoked potentials , evoked potential , toxic encephalopathy , chemistry , convulsion , anesthesia , galactosamine , medicine , encephalopathy , neuroscience , biology , biochemistry , audiology , epilepsy , cirrhosis , physics , optics , glucosamine
Visual evoked potentials were utilized to examine the neuronal transmission changes provoked by galactosamine‐induced hepatic encephalopathy and by administration in normal animals of toxins presumably involved in the pathogenesis of hepatic encepalopathy. Separate acute administrations of ammonia, dimethyldisulfide, and octanoic acid induced lethargy, convulsions in the case of the first two, and coma with visual‐evoked potential patterns that never resembled the evoked potentials recorded in hepatic coma. By contrast, single and repeated administrations of the three above‐mentioned toxins together at lower doses induced lethargy and coma with visual‐evoked potential patterns similar to those observed in galactosamine‐induced hepatic coma. These observations, together with previously published data, are consistent with the concept that the synergistic interaction of these toxins plays a significant role in the pathogenesis of hepatic encephalopathy.