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Catecholamine and octopamine concentrations in brains of patients with Reye syndrome

Department of Psychopharmacology, Clarke Institute of Psychiatry (K. G. Lloyd, L. Davidson, and K. Price), Department of Pharmacology, University of Toronto (K. G. Lloyd), Children's Hospital, Columbus, Ohio (H. J. McClung) and the Hospital for Sick Children, Toronto (D. G. Gall).

Dopamine, norepinephrine, and octopamine levels were estimated in regions of brains obtained postmortem from children who died with Reye syndrome and from age-matched controls. Hypothalamic norepinephrine levels were greatly decreased (to 30 percent of control, p < 0.02) and octopamine levels were increased (to 700 percent of control, p < 0.01). Levodopa had little effect on the physiologic condition of the patients. However, CNS dopamine and homovanillic concentrations were not elevated by levodopa, indicating that in the present cases levodopa was not metabolized to its catecholamine products. The findings indicate that the encephalopathy of Reye syndrome (as in other types of hepatic coma) may be linked to the presence of false transmitters in the brain and that levodopa is a rational therapy if administered before irreversible CNS changes occur.

Dr. Lloyd's address is Depactment of Psychopharmacology, Clarke Institute of Psychiatry, 250 College Street, Toronto, Ontario, Canada, M5T 1R8.

This work was supported by a grant from the Hospital for Sick Children Foundation and by the Clarke Institute of Psychiatry and the Hospital for Sick Children, Toronto, Canada.

Accepted for publication November 1976.