Vitamin E for neuroleptic-induced tardive dyskinesia

Enhance Reviews Ltd, John Eccles House, Robert Robinson Avenue, Oxford Science Park, Oxford, UK, OX4 4GP.
Cochrane database of systematic reviews (Online) (Impact Factor: 5.94). 01/2011; DOI: 10.1002/14651858.CD000209.pub2
Source: PubMed

ABSTRACT Antipsychotic (neuroleptic) medication is used extensively to treat people with chronic mental illnesses. Its use, however, is associated with adverse effects, including movement disorders such as tardive dyskinesia (TD) - a problem often seen as repetitive involuntary movements around the mouth and face. Vitamin E has been proposed as a treatment to prevent or decrease TD.
To determine the effects of vitamin E for people with schizophrenia or other chronic mental illnesses who also developed neuroleptic-induced TD.
We searched the Cochrane Schizophrenia Group Trials Register (March 2010), inspected references of all identified studies for further trials and contacted authors of trials for additional information.
We included reports if they were controlled trials dealing with people with neuroleptic-induced TD and schizophrenia who had been randomly allocated to either vitamin E or to a placebo or no intervention.
We independently extracted data from these trials and we estimated risk ratios (RR) or mean differences (MD), with 95% confidence intervals (CI). We assumed that people who dropped out had no improvement.
The review now includes 11 poorly reported randomised trials (total 427 people). There was no clear difference between vitamin E and placebo for the outcome of 'clinically relevant improvement in TD' (6 trials, 256 people, RR 0.95 CI 0.89 to 1.02). For the outcome of 'any improvement in TD symptoms', again, we found no clear difference between groups (7 trials, 311 people, RR 0.86 CI 0.75 to 1.00). However, people allocated to placebo showed more deterioration of their symptoms compared with those given vitamin E (5 trials, 98 people, RR 0.38 CI 0.16 to 0.9). There was no difference in the incidence of adverse effects (9 trials, 203 people, RR 1.29 CI 0.51 to 3.24) or leaving the study early (medium term 6 trials, 173 people, RR 1.29 CI 0.72 to 2.3). There is no trial-based information regarding the effect of vitamin E for those with early onset of TD.
Small trials of limited quality suggest that vitamin E may protect against deterioration of TD. There is no evidence that vitamin E improves symptoms of this problematic and disfiguring condition once established. New and better trials are indicated in this under-researched area, and, of the many adjunctive treatments that have been given for TD, vitamin E would be a good choice for further evaluation.

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