Long-term treatment effects of vitamin E for tardive dyskinesia

Psychiatry Service, New York Department of Veterans Affairs Medical Center, New York, USA.
Biological Psychiatry (Impact Factor: 10.26). 07/1998; 43(12):868-72. DOI: 10.1016/S0006-3223(97)00027-9
Source: PubMed


Several studies have found that alpha-tocopherol (vitamin E) can effectively treat tardive dyskinesia (TD). A limitation of these trials is their short treatment durations (maximum of 12 weeks), which do not allow us to address the effects of long-term treatment.
To participate, patients had to have TD and be on stable oral medications. The study enrolled 40 patients who received up to 36 weeks of treatment with d-vitamin E (1600 IU per day) or placebo.
Using the Abnormal Involuntary Movements Scale (AIMS) score (sum of items #1-7) to measure TD severity, the study found a significant difference (3 points) in mean AIMS scores, in favor of vitamin E, starting at 10 weeks of treatment and continuing through the full 36 weeks. We used linear mixed-effects regression to quantify the impact of several covariates, and found that treatment assignment. TD duration, and chlorpromazine equivalents had significant effects on decreasing the AIMS score.
The study's finding that vitamin E is effective in treating TD agrees with results from prior studies and provides evidence that the effect may extend to treatment of up to 36 weeks. These findings are in direct contrast to those of VA Cooperative Study #394, a much larger, long-term, multi-site study, conducted by many of the same investigators, in which Vitamin E was not superior to placebo.

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    • "some efficacy, which also provide indirect evidence for a role of free radicals in TD (Lohr et al., 1988; Egan et al., 1992; Adler et al., 1993, 1998; Lohr and Caligiuri, 1996). However, more recently, the result in a large-scale Veterans Affairs Cooperative study showed that vitamin E was not superior to placebo (Adler et al., 1998). Recently, superoxide dismutase (SOD), a key enzyme involved in the detoxification of superoxide radicals has been found to be lower in both erythrocyte and CSF in patients with TD (Yamada et al., 1997; Tsai et al., 1998). "
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    ABSTRACT: Free radicals may be involved in the pathogenesis of tardive dyskinesia (TD). Superoxide dismutase (SOD), a critical enzyme in the detoxification of superoxide radicals, was found to be abnormal in TD. To examine the blood SOD levels in schizophrenic patients with and without TD, and the relationships between SOD levels and tardive dyskinesia symptoms in TD patients, 45 physically healthy patients with TD who met DSM-III-R criteria for schizophrenia were compared with 45 schizophrenic patients without TD, as well as with 50 age-, sex- and smoking-matched normal controls. The severity of TD was assessed using the abnormal involuntary movement scale (AIMS). The psychopathology of patients were assessed by the Positive and Negative Syndrome Scale (PANSS). Blood SOD levels were measured by radioimmunometric assay (RIA). The results showed that the patients with TD had lower concentrations of blood SOD than those without TD, but had higher blood SOD levels than the normal controls. In the patients with TD, AIMS total score was inversely correlated with SOD levels. Our data support the view that free radicals may be involved in the pathophysiology of TD. There may exist a relationship between the free radical metabolism and the severity of dyskinesia of TD patients.
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    • "Recent data suggest the possibility that the newer antipsychotics present a much lower risk for movement disorder, even in older patients, and that the development of tardive dyskinesia may be preventable through use of different medication (Katz et al. 1999). Similarly, trials of agents (antioxidants, for example) hypothesized to treat these side effects have been proposed, though the data from some of the early studies have been inconsistent (Adler et al. 1998; Lohr and Lavori 1998). It is at least possible, however, to consider that these studies should have been designed as prevention trials rather than treatment trials, with the subjects being those with a first exposure to neuroleptics who would then be randomized to receive vitamin E in addition. "
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