Current pathogenetic aspects of hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy

Abstract

Hepatic encephalopathy is a medical phenomenon that is described as a neuropsychiatric manifestation of chronic or acute liver disease that is characterized by psychomotor, intellectual and cognitive abnormalities with emotional/affective and behavioral disturbances. This article focuses on the underlying mechanisms of the condition and the differences between hepatic encephalopathy and noncirrhotic hyperammonemic encephalopathy. Hepatic encephalopathy is a serious condition that can cause neurological death with brain edema and intracranial hypertension. It is assumed that approximately 60%-80% of patients with liver cirrhosis develop hepatic encephalopathy. This review explores the complex mechanisms that lead to hepatic encephalopathy. However, noncirrhotic hyperammonemic encephalopathy is not associated with hepatic diseases and has a completely different etiology. Noncirrhotic hyperammonemic encephalopathy is a severe occurrence that is connected with multiple pathogeneses.

Keywords: Ammonia; Astrocyte; Hepatic encephalopathy; Noncirrhotic hyperammonemic encephalopathy; Oxidative stress; Pathogeneses.

Figure 1

The different factors and mechanisms involved in the pathogenesis of hepatic encephalopathy. GABA: Gamma-aminobutyric acid; NMDA: N-methyl-D-aspartate.