Vitamin E for neuroleptic-induced tardive dyskinesia

Having to take antipsychotic drugs for long periods of time can cause repetitive movements - often of the face and mouth. These are disfiguring and do not necessarily cease once medication is reduced or changed. Vitamin E has been evaluated for treating these movement disorders, but, so far, the benefit of this medication seems small and restricted to avoidance of deterioration.

Authors' conclusions: 

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.

Read the full 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.

Search strategy: 

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.

Selection criteria: 

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.

Data collection and analysis: 

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.

Main results: 

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.