The chapter discusses recent progress, concerning the role of astrocytes in hepatic encephalopathy (HE). New concepts regarding the role of second messengers (cyclic AMP and Ca2+) and protein phosphorylation are discussed. Data on glycogen metabolism that are especially pertinent to a potential defect in glial-neuronal communication is presented. Finally, discussion on derangements in cytoskeletal proteins, volume regulation, and the involvement of the peripheral type benzodiazepine receptor is given. HE occurs in two clinical forms: acute or fulminant hepatic failure (FHF) and chronic (portal-systemic encephalopathy, PSE). FHF, generally occurring in the setting of viral or toxic hepatitis, usually presents with the rapid onset of delirium, coma, and seizures. PSE on the other hand, manifests initially with subtle personality changes, confusion, episodic stupor, and when severe with coma.
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