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Monroe Cole, MD; Robert B. Rutherford, MD; Forrest Owen Smith, MD

Arch Neurol. 1972;26(2):130-136.

Abstract
The role of ammonia in hepatic encephalopathy has never been clearly defined. We have approached the problem by constant infusion of macaques with ammonium acetate. Controls consisted of non-infused and sodium-acetate-infused animals, as well as animals with a portacaval shunt. Achieving blood ammonia levels of 200µg to 400mµg 100 ml for periods of 2 to 44 days, we have produced a clinicopathologic syndrome reasonably similar to that seen in patients dying of hepatic encephalopathy. Pathologic changes in the brain consisted of a proliferation of astrocytes in gray matter, mainly of the protoplasmic variety. Lethargy and stupor occurred for short periods in some animals. The electroencephalographic abnormality consisted of diffuse symmetrical slow activity and could be related to the presence of gliosis. We conclude that ammonia is toxic to the brain at levels ordinarily seen in the clinic.

Author Affiliations
Washington, DC

From the divisions of neurophysiology and experimental surgery, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, DC.

Footnotes
Accepted for publication Sept 17, 1971.

Read before the 95th annual meeting of the American Neurological Association, Atlantic City, NJ, June 16, 1970.

Reprint requests to Department of Neurology, Highview Hospital, 3901 Ireland Dr, Cleveland 44122 (Dr. Cole).

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