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Psychometric tests were administered to 36 alcoholic patients with cirrhosis without overt portal systemic encephalopathy and to 32 alcoholics without liver diseases. Verbal ability was preserved in both groups. The cirrhotic patients scored worse than the alcoholics without liver disease on most of the tests of psychomotor performance. Based on the three most discriminative tests, 50% of the cirrhotic patients had one or more scores that were more abnormal than those of any member of the alcoholic group. Significant correlations were found between the severity of liver disease and most tests of performance in the cirrhotic group, due primarily to the influence of serum albumin as a component of the severity index. We conclude that psychomotor tests are sensitive tools for the detection of latent encephalopathy, and that nutritional status probably plays a role in determining test performance.

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SUMMARY Blood methanethiol and ammonia concentrations were measured in 16 healthy volunteers, 52 consecutive alcoholic cirrhotics without overt hepatic encephalopathy (HE), and 42 consecutive patients with alcoholic liver disease and overt HE. The mean concentration of blood methanethiol was significantly greater than normal in the cirrhotics without overt HE, and the means of both methanethiol and ammonia were significantly greater in the patients with than in those without overt HE. Only one patient with overt HE had both normal ammonia and methanethiol blood concentrations. Twenty of the patients with HE were followed serially. The directions of change in methanethiol and ammonia were consistent with the direction of change in mental status in 85 % and 60 % respectively. All of the patients who deteriorated and died had changes in blood methanethiol that correlated with the change in mental status. We conclude that blood methanethiol is a valuable adjunct to the ammonia determination in the evaluation of the patient with possible HE. It is especially helpful in following the course of a patient with hepatic encephalopathy, both as to prognosis and as an indicator of response to therapy. Mercaptans are extremely toxic sulphur-containing compounds that appear to be largely derived from colonic bacterial metabolism of methionine. Like ammonia, mercaptans are normally efficiently removed by the liver but escape detoxification with hepatic failure or shunting of intestinal blood around the liver. Animal studies have shown that small amounts of mercaptans can cause reversible coma and can act synergistically with ammonia and fatty acids to enhance the toxicity of these substances.' In 1955, Challenger and Walshe2 established the association of mercaptans with hepatic failure by isolating methanethiol (methyl mercaptan) from the urine of a woman in deep hepatic coma, and, in 1970, Chen and his colleagues3 reported a four-fold increase in breath methanethiol in patients with hepatic failure. Recently, a method for measuring mercaptans was developed that was sufficiently sensitive to detect methanethiol in the blood of patients for the first time.4 We have applied this method to patients with hepatic failure over the past two years and are now reporting the results of this initial experience.