Hepatic encephalopathy: A disorder in glial-neuronal communication

M. D. Norenberg, J. T. Neary, A. S. Bender, R. S. Dombro

Research output: Contribution to journalArticle

49 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)261-269
Number of pages9
JournalProgress in brain research
Volume94
Issue numberC
DOIs
StatePublished - Jan 1 1992

ASJC Scopus subject areas

  • Neuroscience(all)

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