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Visual Evoked Potentials in Encephalopathy Induced by Galactosamine, Ammonia, Dimethyldisulfide, and Octanoic Acid

Authors

  • Maria L. Zeneroli,

    Corresponding author
    1. Istituti di Semeiotica Medica e di Farmacologia, Clinica Oculistica, Modena University, via del Pozzo, 41100 Modena, Italy, and Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota 55415
    • Maria L. Zeneroli, M.D., Instituti di Semeiotica Medica, Modena University, via del Pozzo, 41100 Modena, Italy.
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  • Ezio Ventura,

    1. Istituti di Semeiotica Medica e di Farmacologia, Clinica Oculistica, Modena University, via del Pozzo, 41100 Modena, Italy, and Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota 55415
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  • Mario Baraldi,

    1. Istituti di Semeiotica Medica e di Farmacologia, Clinica Oculistica, Modena University, via del Pozzo, 41100 Modena, Italy, and Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota 55415
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  • Alessandro Penne,

    1. Istituti di Semeiotica Medica e di Farmacologia, Clinica Oculistica, Modena University, via del Pozzo, 41100 Modena, Italy, and Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota 55415
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  • Elena Messori,

    1. Istituti di Semeiotica Medica e di Farmacologia, Clinica Oculistica, Modena University, via del Pozzo, 41100 Modena, Italy, and Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota 55415
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  • Leslie Zieve

    1. Istituti di Semeiotica Medica e di Farmacologia, Clinica Oculistica, Modena University, via del Pozzo, 41100 Modena, Italy, and Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota 55415
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Abstract

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.

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