Cognitive Function of Alcoholic Compensated Liver Cirrhosis
Cognitive Function of Alcoholic Compensated Liver Cirrhosis
Differences in cognitive function between patients with viral and 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.
Inclusion Criteria:

 -  Those who agreed to participate in this study and signed a written consent

 -  Those who have no evidence of neurological impairment

 Exclusion Criteria:

 -  Those who have decompensated liver cirrhosis

 -  Those who have a high MELD score (≥20)

 -  Those who have OHE during admission

 -  Those who have parients' refusal