For many years, coma—often prolonged—has been described as a common prelude to the death of patients with liver disease. This altered state of consciousness has been known as hepatic coma (probably a better term than "liver coma," which presumes a prior conscious state for the organ). The pathogenesis was little understood, nor was it investigated until Adams, Foley, and their colleagues,1,2 by careful neurological study of patients, provided a clinical description of the syndrome in all its stages and made it possible to detect the early signs of the condition. This advance has awakened interest in investigation of the relationship of ammonia to the syndrome, already suggested by Kirk,3 van Caulaert,4 Fuld,5 and others. The results have been a multitude of studies and papers on the subject (as could have been expected) and a welter of terms for the syndrome. The purpose here is to view critically some of these
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