Abstract
Fenclonine (DL-parachlorophenylalanine), a potent inhibitor of serotonin synthesis, was administered to six patients with Huntington's chorea. Doses sufficient to reduce the cerebrospinal fluid (CSF) content of 5-hydroxyindoleacetic acid (5-HIAA), the principal catabolite of serotonin by nearly 50%, produced no consistent alteration in motor or behavioral function. The pretreatment concentration of 5-HIAA in CSF was in the normal range. Cerebrospinal fluid levels of homovanillic acid, a major catabolite of dopamine, did not change during drug treatment. The results thus fail to support the hypothesis that hyperfunction of serotonin-containing neural systems plays a crucial role in the pathogenesis of Huntington's disease.
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