Pathophysiology of hepatic encephalopathy.
Changes in various neurotransmitter systems, in blood brain barrier integrity and/or function, and in brain energy metabolism, may precipitate HE. Although a "specific cause" of HE (i.e. the presence of a well-defined toxin) has not been identified so far, the common denominator of all these changes is the presence of liver failure. The various hypotheses of the pathogenesis of HE are not mutually exclusive, but have to be integrated into the clinical syndrome of liver failure. It is conceivable that "specific causes" of HE do not exist at all. Brain function may be affected to a certain degree by the various consequences of liver failure (such as the accumulation of neuroactive compounds and of neurotoxins, changes in the metabolism of amino acids, decreased availability of energy fuels and circulatory changes), finally precipitating the syndrome of HE.
Department of Gastroenterology and Hepatology, University of Vienna, Austria.
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D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000378:metabolism; D002395:Catecholamines / Q000502:physiology; D004734:Energy Metabolism; D005971:Glutamates / Q000502:physiology; D018698:Glutamic Acid; D006501:Hepatic Encephalopathy / Q000503:physiopathology*; D006801:Humans; D009498:Neurotoxins; D012701:Serotonin / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D002395:Catecholamines; D005971:Glutamates; D009498:Neurotoxins; D012701:Serotonin; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid