There are several reports regarding the efficacy of
vitamin B6 in the treatment of
tardive dyskinesia (TD).
Vitamin B6 plays a key role in the synthesis of several
neurotransmitters, including
serotonin,
dopamine,
norepinephrine, and
gamma-aminobutyric acid, all of which have been proposed to be involved in the development of TD. The purpose of this study was to examine whether there are special markers to distinguish long-term
neuroleptic exposure patients who have TD from those patients who do not develop this side effect. In view of the pivotal role of
vitamin B6 in the synthesis of all
neurotransmitters believed to take part in the pathogenesis of TD, we decided to examine whether basal levels of
vitamin B6 might explain the difference between these two groups. Such a finding could provide a predictive marker for vulnerable patients. The active metabolite of
vitamin B6 is
pyridoxal phosphate (PP).
Pyridoxal phosphate blood levels were measured in 15 schizophrenic and schizoaffective patients with TD and compared with 15 patients without evidence of TD (matched by sex, age, smoking, and diagnosis). We found that, although patients in the TD group were exposed to
neuroleptic drugs for significantly longer periods of time, there were no differences in serum PP levels between the groups. The reports of the effectiveness of
vitamin B6 supplementation in the treatment of TD could therefore be explained by the assumption that central nervous system or intracellular
vitamin B6 levels, which are involved in the pathogenesis of TD, are not the same as
vitamin B6 peripheral serum levels. There is need for further studies, which will clarify the relationship between
vitamin B6 and TD.