Cognitive Function of Alcoholic Compensated Liver Cirrhosis

Hepatic encephalopathy (HE) is one of the important complications of liver cirrhosis (LC). HE exhibits alterations in cognitive, psychomotor-intellectual, emotional, behavioral, or fine-motor functions. Approximately 22-74 % of patients with non-fulminant HE have MHE with a frequency proportional to the patient age and the severity of the liver disease. Patients with MHE exhibit disability in most functional behaviors such as social connection, alertness, emotional behavior, sleep, work, and leisure. Alcohol consumption itself has a toxic effect on the brain. It has been documented that there is a neuronal loss in the cerebral cortex, hypothalamus, hippocampus, septal region, and cerebellum of an alcoholic brain. The major causes of LC are hepatitis B/C viral infection and chronic alcohol consumption. The most widely accepted theory of HE pathogenesis is that toxic substances derived from the gut affect cerebral function after liver dysfunction or portosystemic shunting. This proposed pathogenetic mechanism could apply to viral compensated LC. However, it is difficult to explain the development of MHE in patients with alcoholic LC in this manner. Therefore, patients with alcoholic LC may have different cognitive dysfunction as compared to patients with viral LC.