Hepatic encephalopathy can develop acutely, complicating fulminant hepatic failure or progress slowly, complicating chronic cirrhosis or portocaval shunt. A disorder of the metabolism of nitrogen and ammonia levels in the blood are involved in pathogenesis. Acquired diseases NEUROMETABOLIC / 203 presents with acute hepatic encephalopathy weathered out, delusional state, convulsions and signs of intracranial hypertension progresses rapidly to coma and death. Chronic hepatic encephalopathy present with minor behavioral abnormalities, mental dullness, asterixis, extrapyramidal symptoms, cerebellar ataxia and dysarthria. End-stage implementation progresses gradually altered to stupor and coma. The blood ammonia level is high. EEG abnormalities consist of Figure 10.5 Subacute combined degeneration of the spinal cord in vitamin B12 deficiency. Macrosection of lumbar spinal cord shows spongy degeneration of myelin in the posterior columns and cortex areas of the sidebars. paroxysms of bilaterally synchronous slow waves or triphasic in the delta range. Pathology: Grossly, in acute hepatic encephalopathy, the brain is swollen and may have a greenish tint of bilirubin through the disrupted blood-brain barrier. In chronic encephalopathy, brain atrophy is variable. Histologically, acute and chronic encephalopathies are characterized by the presence of Alzheimer’s disease type 2 astroglia. These astrocytes have a large, round, or lobulated nucleus crescentshaped less often with vesicular chromatin and prominent nucleoli rare. Perikarya do not stain with eosin. They are generally immunonegative for GFAP, but immunopositive for S-100 protein, and may contain inclusions of glycogen. These astrocytes are found in the deeper layers of the cortex, basal ganglia, thalamus and dentate and olivary nuclei. Other features of hepatic encephalopathy are chronic and microvacuolation necrosis in the cerebral cortex at the junction with the white matter and basal ganglia and cerebellum.