Peripheral nerve function may be impaired in chronic liver disease. The incidence of demyelinating neuropathy was reported to be between 20 to 90 percent in various electrophysiologic and histopathologic studies. However after elimination of alcoholism and diabetes mellitus, this rate is reported to decrease to 6 percent. Most cases are asymptomatic, but there are rare cases with serious neuropathic symptoms. Although the exact cause of peripheral neuropathy in cirrhosis is not known, toxic metabolites are thought to be responsible. In this study, we have investigated 21 patients (14 female, 7 male) with non-alcoholic cirrhosis. All patients had Child-C cirrhosis. Cirrhosis was diagnosed by clinical, laboratory and endoscopic means, and confirmed by liver biopsies. Serum folic acid, vitamin B12 and ammonia levels were determined. Patients with alcoholism, diabetes mellitus and hepatic encephalopathy, and those taking drug that might have caused peripheral neuropathy were excluded. Conduction velocity of two motor and sensory nerves were measured by Nihon Kohden Neuropack 8 apparatus in the upper and lower extremities. The results were compared with normal values obtained in our clinic. Slowing of the conduction velocity that indicate demyelinating sensorimotor polyneuropathy was defined in 7 (%33.3) cases. Prothrombin time of patients with defined neuropathy teas found to be longer and alkaline phosphatase and globulin values to be higher than in those without neuropathy (p < 0.05).