Ammonia : this is not the end but rather the end of the beginning

Abstract

Hepatic encephalopathy (HE) represents a wide spectrum of neurological or neuropsychological symptoms caused by liver disease and/or portosystemic shunts. The major role of hyperammonemia in association with systemic inflammation and oxidative stress in the pathogenesis of HE has progressively emerged. However, the cascading downstream effects caused by these pathogenic factors remain unresolved. The underlying abnormalities which are thought to cause HE include modification of glutamatergic and GABAergic neurotransmission, mitochondrial dysfunction, energy impairment, lactate dyshomeostasis, increased blood-brain barrier permeability, brain edema/astrocyte swelling, as well as accumulation of toxic compounds (manganese, bile acids, indols).