<i>L</i>-Dopa, B₆, and <i>α</i>-Methyldopa Hydrazine

Abstract

It has been suggested that L-dopa combines with pyridoxine (B₆) to form a specific antiparkinsonian molecule. This raises the possibility that the efficacy of L-dopa can be increased by giving patients both L-dopa and vitamin B₆. The administration of B₆ to parkinsonian patients receiving L-dopa reverses the L-dopa effect. It has been suggested that the L-dopa effect is not reversed by B₆ in patients receiving both L-dopa and a peripheral dopa decarboxylase inhibitor; thus, it is possible that administration of B₆ in large doses to patients receiving this combination might increase the antiparkinsonian efficacy of L-dopa. To systematically evaluate this possibility, 12 patients receiving oral L-dopa and α-methyldopa hydrazine (MK-486), a peripheral dopa decarboxylase inhibitor, were given pyridoxine daily for 5–10 days. This failed to increase the antiparkinsonian effect of L-dopa in all 12 patients. It also failed to reverse the L-dopa effect or alter any of the side effects. The failure of B₆ to reverse the dopa effect confirms the concept that B₆ reversal involves peripheral dopa decarboxylase. The failure of large amounts of B₆ to increase the L-dopa effect casts doubt on the concept that a Schiff base formed of L-dopa and B₆ is the specific antiparkinsonian agent mediating the effect of L-dopa.