K V Soares1, J J McGrath. 1. Dov Hoz Street, 27/16, Kfar Saba, Israel, 44356. ksoares@netvision.net.il
Abstract
BACKGROUND: Neuroleptic (antipsychotic) 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 (1982-1998), The Cochrane Schizophrenia Group's Register (September 1998), EMBASE (1980-98), LILACS (1982-96), MEDLINE (1966-98), PsycLIT (1974-98), SCISEARCH, handsearching 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 Peto odds ratios (OR) or average differences, with the 95% confidence intervals (CI) were estimated. The reviewers assumed that people who dropped out had no improvement. MAIN RESULTS: Eight studies were included, and another three are currently awaiting further data from authors. The overall results for both, 'clinically relevant improvement' and 'any improvement' of TD symptoms, were in favour of vitamin E (OR 0.16, CI 0.04-0.7, NNT 5 CI 2.-32 and OR 0.23, CI 0.10-0.55, NNT 4 CI 2. 5-12 respectively). People who had not used vitamin E showed more deterioration of their symptoms (OR 0.20, CI 0.04-0.93). No difference could be found regarding the presence of adverse effects or leaving the study early before the end of study. 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, tend to suggest that vitamin E improves the symptoms of TD. Methodological problems such as small sample size, short term interventions, and inappropriate use of crossover design need to be dealt with in any future studies. The results of a recently completed trial involving 158 participants are eagerly awaited.
BACKGROUND: Neuroleptic (antipsychotic) 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 (1982-1998), The Cochrane Schizophrenia Group's Register (September 1998), EMBASE (1980-98), LILACS (1982-96), MEDLINE (1966-98), PsycLIT (1974-98), SCISEARCH, handsearching 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 Peto odds ratios (OR) or average differences, with the 95% confidence intervals (CI) were estimated. The reviewers assumed that people who dropped out had no improvement. MAIN RESULTS: Eight studies were included, and another three are currently awaiting further data from authors. The overall results for both, 'clinically relevant improvement' and 'any improvement' of TD symptoms, were in favour of vitamin E (OR 0.16, CI 0.04-0.7, NNT 5 CI 2.-32 and OR 0.23, CI 0.10-0.55, NNT 4 CI 2. 5-12 respectively). People who had not used vitamin E showed more deterioration of their symptoms (OR 0.20, CI 0.04-0.93). No difference could be found regarding the presence of adverse effects or leaving the study early before the end of study. 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, tend to suggest that vitamin E improves the symptoms of TD. Methodological problems such as small sample size, short term interventions, and inappropriate use of crossover design need to be dealt with in any future studies. The results of a recently completed trial involving 158 participants are eagerly awaited.