Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 16 patients with hepatic encephalopathy before and/or after treatment. CSF lactate was significantly increased to 1.92 ± 0.11 mmol/1 in hepatic encephalopathy before the treatment in comparison to 1.40 ± 0.05 mmol/1 in control subjects. In 9 of 11 patients with moderate or stage 2 encephalopathy, CSF lactate levels were below 2 mmol/1. In contrast, in 4 of 5 patients with stage 3–4 encephalopathy, CSF lactate levels were higher than 2 mmol/1. CSF lactate was decreased with the recovery of neurological symptoms by the treatment. These findings indicate that CSF lactate levels reflect the severity of metabolic impairment of the brain. Hypocapnia was frequently observed in these encephalopathic patients, and arterial Pco2 correlated inversely with CSF lactate and linearly with CSF HCO–3, suggesting that CSF lactic acidosis contributes to hyperventilation in hepatic encephalopathy. It is concluded from present results that metabolic disorder of neuronal cells might be one of the important factors for the development of hepatic encephalo