Abstract
Studies on the pathogenesis of hepatic encephalopathy (HE) following fulminant hepatic failure (FHF) have focused on biochemical changes occurring in blood, in cerebrospinal fluid or in brain with the aim of recognizing the primary factors leading to the central nervous system (CNS) dysfunction of coma. Because of the numerous metabolic abnormalities found in this pathology a congeries of theories has been generated, but none of these is so fully proved as to be accepted.
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© 1984 Plenum Press, New York
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Zeneroli, M.L., Baraldi, M., Ventura, E. (1984). γ-Aminobutyric Acid Receptors in Experimental Hepatic Encephalopathy. In: Capocaccia, L., Fischer, J.E., Rossi-Fanelli, F. (eds) Hepatic Encephalopathy in Chronic Liver Failure. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4787-3_4
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DOI: https://doi.org/10.1007/978-1-4684-4787-3_4
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