Abstract
Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver before toxins are removed. As a result, toxins such as ammonia and manganese can accumulate in the blood and enter the brain, where they can damage nerve cells and supporting cells called astrocytes. Positron emission tomography analyses have determined that ammonia levels are elevated in the brains of HE patients; ammonia accumulation can alter the expression of various important brain genes. Magnetic resonance images show that manganese is deposited in a brain area called the globus pallidus; manganese deposits may be responsible for structural changes in the astrocytes that are characteristic of HE. Treatment of patients with HE involves measures to lower ammonia levels in the blood, medications to counteract ammonia's effects on brain cell function, devices to compensate for liver dysfunction, and liver transplantation.
MeSH Terms
Brain/pathology
Hepatic Encephalopathy/diagnosis,genetics,therapy
Humans
Liver Diseases, Alcoholic/diagnosis,genetics,therapy
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Butterworth Roger F
Neuroscience Research Unit, CHUM (Hôpital Saint-Luc), Montreal, Canada.
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