Hepatic encephalopathy: a disorder in glial-neuronal communication.
作者： M.D. Norenberg , J.T. Neary , A.S. Bender , R.S. Dombro
DOI: 10.1016/S0079-6123(08)61756-2
关键词:
摘要: Publisher Summary The chapter discusses recent progress, concerning the role of astrocytes in hepatic encephalopathy (HE). New concepts regarding second messengers (cyclic AMP and Ca2+) protein phosphorylation are discussed. Data on glycogen metabolism that especially pertinent to a potential defect glial-neuronal communication is presented. Finally, discussion derangements cytoskeletal proteins, volume regulation, involvement peripheral type benzodiazepine receptor given. HE occurs two clinical forms: acute or fulminant failure (FHF) chronic (portal-systemic encephalopathy, PSE). FHF, generally occurring setting viral toxic hepatitis, usually presents with rapid onset delirium, coma, seizures. PSE other hand, manifests initially subtle personality changes, confusion, episodic stupor, when severe coma.
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