ELEVATED CONCENTRATIONS OF CSF HOMOVANILLIC ACID IN REYE SYNDROME-A POSSIBLE RELATION TO CEREBRAL HYPOPERFUSION

Abstract

Recent investigations suggest a relationship between braindopamine release and subsequent hypoperfusion. Such an association has important therapeutic implications since abundant pharmacological agents are available that could be utilized to modify central monoaminergic mechanisms. We have examined cerebral ventricular fluid concentrations of homovanillic acid(HVA) and 5-hydroxyindoleacetic acid (5-HIAA), the principal metabolites of dopamine and serotonin respectively, in 7 children with Reye syndrome. In these children, CSF was obtained during continuous intracranial pressure (ICP) monitoring and compared with ventricular CSF from 6 children with communicating hydrocephalus. Maximum HVA (ng/ml, mean ± SEM) was significantly elevated in Reye syndrome averaging 1140 ± 313 compared to 267 ± 64.5 in controls (p < 0.005) while 5-HIAA was similar, averaging 232 ± 32.5 and 187 ± 33.9 in Reye syndrome and controls respectively (p > 0.10). Peak HVA concentration occurred 1-2 days after the maximum blood NH3; however, there was no significant correiation between the maximum CSF concentration of either HVA or 5-HIAA and maximum blood NH3. ICP was increased in all children with Reye syndrome but there was no consistent pattern between HVA concentration and degree of ICP elevation. Our findings suggest a sequence of dopamine release (as reflected by elevations in HVA), cerebral vasoconstriction, and a resultant hypoperfusion in Reye syndrome.