Although there are similarities between the encephalopathy of acute hepatic failure and that due to cirrhosis, it is clear that some of the biochemical abnormalities arise in different ways and the relative roles of the various factors contributing to the production of encephalopathy may differ. in addition, in fulminant hepatic failure, changes in the permeability of the blood—brain barrier may enhance the effects of biochemical abnormalities and this may also be important in the genesis of cerebral oedema, which commonly complicates this form of encephalopathy. When considering encephalopathy complicating cirrhosis, it is important to recognize that the latter can be precipitated by a variety of insults each of which may lead to encephalopathy. Most research has concentrated on the accumulation in the blood of ‘toxic’ substances normally metabolized by the liver. Although no single toxin has yet been identified which alone can be responsible for hepatic encephalopathy, excess ammonia, mercaptans, fatty acids and an abnormal plasma amino acid profile have been incriminated in its pathogenesis. Irrespective of the ‘toxin’, three main pathogenetic mechanisms have been proposed to account for its action: (a) disturbed brain energy metabolism, (b) deranged neurotransmitter balance, (c) direct effects on neuronal membranes. These mechanisms are not regarded as mutually exclusive but have their final common effect of interrupting normal neurotransmission.

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