Background. Cocaine acts in the central nervous system by increasing dopamine release and inhibiting the reuptake of dopamine and other monoaminergic neurotransmitters. Prenatal cocaine exposure may cause neurochemical changes in developing monoaminergic neurons and might alter brain structure and function. No data have been published on central nervous system monoamine precursors and metabolites in human neonates exposed prenatally to cocaine. Methods. Cerebrospinal fluid (CSF) was obtained from neonates undergoing lumbar puncture to rule out infection. The CSF was analyzed for the neurotransmitter precursors and metabolites tryptophan, tyrosine, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, and 5-hydroxyindoleacetic acid. Drug exposure was ascertained by medical record review and urine and meconium assays. Results. Eleven neonates were cocaine-exposed, based on positive meconium or urine assays for benzoylecgonine; 20 were unexposed, based on both negative history and assay. The exposed and unexposed groups did not differ significantly in gender, perinatal stress, clinical illness, or exposure to other illicit drugs, but did differ in mean gestational age, growth parameters, and exposure to cigarettes. Cocaine-exposed neonates had significantly lower levels of CSF homovanillic acid (mean 148.1 vs 218.5 ng/mL, P = .01). The magnitude of this difference was similar after correcting for each of four potential confounding factors, although no longer statistically significant in all cases (P values ranged from .044 to .17). No significant differences were observed for tyrosine, tryptophan, 5-hydroxyindoleacetic acid, or 3-methoxy-4-hydroxyphenylglycol. Conclusions. These preliminary results suggest an association between prenatal cocaine exposure and decreased CSF homovanillic acid, the principal metabolite of dopamine. Prenatal cocaine exposure may result in changes in central dopaminergic systems in the human neonate.
It was accidentally observed that monkeys receiving a diet which included a banana on the final day of an experimental period suddenly excreted a many-fold increase of 5-hydroxyindoleacetic acid (5-HIAA) in the 24-hour urine collection corresponding to the addition of the banana to the experimental diet. This chance observation was consistently confirmed, and it was found that feeding of 50 to 150 gm of banana resulted in 5 to 30 times as much excretion of 5-HIAA as was excreted in control periods when banana was not included in the diet. Aside from intrinsic interest, this observation is of importance because heretofore increased excretion of 5-HIAA has been observed in the urine of patients with carcinoid tumors and in no other clinical condition in man. No previous reports have shown any influence of dietary constituents other than tryptophan in producing such a striking increase in excretion of 5-HIAA. Administration of iproniazid resulted in a marked reduction in the excretion of 5-HIAA by monkeys being fed banana, just as it does in the case of excretion of 5-HIAA in the urine of patients with carcinoid tumors. At the time of this preliminary report, the ingredient in banana responsible for the increased urinary excretion of 5-HIAA had not been identified, but it is not tryptophan. Elimination of bacteria from the intestinal tract by means of neomycin did not influence the excretion of 5-HIAA in monkeys due to banana in the diet. The effect of banana in the diet on urinary excretion of 5-HIAA was confirmed in two children. This phenomenon is not apt to lead to diagnostic error in children, in whom carcinoid tumors have not been reported, but the importance of application of these findings to diagnosis of carcinoid tumors in adults is apparent.