Pathomechanisms in hepatic encephalopathy
Author:
Häussinger Dieter1, Butz Markus2, Schnitzler Alfons2, Görg Boris1ORCID
Affiliation:
1. Clinic for Gastroenterology, Hepatology, and Infectious Diseases , Heinrich Heine University , Moorenstr. 5 , D-40225 Düsseldorf , Germany 2. Department of Neurology/Institute of Clinical Neuroscience and Medical Psychology, Medical Faculty , Heinrich Heine University , Moorenstr. 5 , D-40225 Düsseldorf , Germany
Abstract
Abstract
Hepatic encephalopathy (HE) is a frequent neuropsychiatric complication in patients with acute or chronic liver failure. Symptoms of HE in particular include disturbances of sensory and motor functions and cognition. HE is triggered by heterogeneous factors such as ammonia being a main toxin, benzodiazepines, proinflammatory cytokines and hyponatremia. HE in patients with liver cirrhosis is triggered by a low-grade cerebral edema and cerebral oxidative/nitrosative stress which bring about a number of functionally relevant alterations including posttranslational protein modifications, oxidation of RNA, gene expression changes and senescence. These alterations are suggested to impair astrocyte/neuronal functions and communication. On the system level, a global slowing of oscillatory brain activity and networks can be observed paralleling behavioral perceptual and motor impairments. Moreover, these changes are related to increased cerebral ammonia, alterations in neurometabolite and neurotransmitter concentrations and cortical excitability in HE patients.
Publisher
Walter de Gruyter GmbH
Subject
Clinical Biochemistry,Molecular Biology,Biochemistry
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