Food and Behaviour Research

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Vitamin E for neuroleptic-induced tardive dyskinesia.

Soares, K.V., McGrath, J.J. (2001) Cochrane Database Syst Rev.  (4) CD000209. 

Web URL: View this abstract (or full text for subscribers) via the Cochrane Library here


BACKGROUND: Antipsychotic (neuroleptic) medication is used extensively to treat people with chronic mental illnesses. However, it is associated with a wide range of adverse effects, including movement disorders such as tardive dyskinesia (TD). Vitamin E has been proposed as a treatment to prevent or decrease the severity of TD.

OBJECTIVES: To determine the clinical effects of vitamin E for people with schizophrenia or other chronic mental illnesses who also developed neuroleptic-induced tardive dyskinesia.

SEARCH STRATEGY: Electronic searches of Biological Abstracts (1982-2001), The Cochrane Schizophrenia Group's Register (January 2001), EMBASE (1980-2001), LILACS (1982-2001), MEDLINE (1966-2001), PsycLIT (1974-2001), SCISEARCH (1997), hand searching the references of all identified studies and contacting the first author of each included trial.

SELECTION CRITERIA: Reports identified in the search were included if they were controlled trials dealing with people with neuroleptic-induced TD and schizophrenia or other chronic mental illness who had been randomly allocated to either vitamin E or to a placebo or no intervention.

DATA COLLECTION AND ANALYSIS: Data were independently extracted from these trials by each reviewer and relative risks (RR) or weighted mean differences (WMD), with 95% confidence intervals (CI) were estimated. The reviewers assumed that people who dropped out had no improvement.

MAIN RESULTS: Ten studies were included. The overall results for 'clinically relevant improvement' found no benefit of vitamin E against placebo (6 trials, 256 people, RR 0.95 CI 0.89 to 1.02). For the outcome of 'any improvement in TD symptoms', again, no clear difference in favour of vitamin E was found (7 trials, 311 people, RR 0.86 CI 0.75 to 1.00). However, people who had not been allocated vitamin E, showed more deterioration of their symptoms (5 trials, 98 people, RR 0.38 CI 0.16 to 0.9). There was no difference in the incidence of adverse effects (8 trials, 163 people, RR 1.3 CI 0.5 to 3.2) or leaving the study early (medium term 5 trials, 133 people, RR 1.5 CI 0.8 to 2.7). There is no trial-based information regarding the effect of vitamin E for those with early onset of TD.

REVIEWER'S CONCLUSIONS: Small trials with uncertain quality of randomisation indicate that vitamin E protects against deterioration of TD but there is no evidence that vitamin E improves symptoms of TD.