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: 6.03). 02/2011; 2(2):CD000209. 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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    • "Early studies showed promising findings in relation to the benefits of Vitamin E for the treatment of tardive dyskinesia (TD) [47–50]. However a recent meta-analysis of 11 RCTs concluded that there is no evidence that Vitamin E improves established TD; although there were limited findings illustrating that Vitamin E supplementation can prevent TD from deteriorating [51]. Therefore, adding Vitamin E to treatment protocols may still be of some benefit to patients experiencing this distressing symptom that can arise from long-term use of anti-psychotic drugs. "
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    ABSTRACT: Schizophrenia is a chronic condition that impacts significantly not only on the individual and family, but the disorder also has wider consequences for society in terms of significant costs to the economy. This highly prevalent condition affects approximately 1% of the worldwide population, yet there are few therapeutic options. The predominant treatment strategy for schizophrenia is anti-psychotic medication (with or without additional talking therapy) even though this approach lacks efficacy in managing the negative symptoms of the condition, is not effective in one-third of the patient group and the side effects of the medication can be severe and debilitating. In recent years, a number of pathophysiological processes have been identified in groups of people with schizophrenia including oxidative stress, one-carbon metabolism and immune-mediated responses. A number of studies have shown that these altered physiological mechanisms can be ameliorated by nutritional interventions in some individuals with schizophrenia. This review briefly describes the aforementioned processes and outlines research that has investigated the utility of nutritional approaches as an adjunct to anti-psychotic medication including antioxidant and vitamin B supplementation, neuroprotective and anti-inflammatory nutrients and exclusion diets. Whilst none of these interventions provides a ‘one-size-fits-all’ therapeutic solution, we suggest that a personalised approach warrants research attention as there is growing agreement that schizophrenia is a spectrum disorder that develops from the interplay between environmental and genetic factors. Electronic supplementary material The online version of this article (doi:10.1186/1475-2891-13-91) contains supplementary material, which is available to authorized users.
    Nutrition Journal 09/2014; 13(1):91. DOI:10.1186/1475-2891-13-91 · 2.60 Impact Factor
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    • "Despite these limitations, this case series suggests that ECT may offer another potential treatment for tardive dystonia and tardive dyskinesia. Controlled studies comparing ECT to current evidenced-based strategies such as vitamin E are warranted.20 Future studies should also include comprehensive measures of cognition. "
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    ABSTRACT: Background Tardive dystonia and dyskinesia are potentially irreversible neurological syndromes. Successful electroconvulsive treatment (ECT) has been reported by multiple sources; however, the existing retrospective reviews and open prospective trials provide little information on the response rate. Methods Eighteen consecutive patients with tardive dystonia or dyskinesia received a standard course of ECT to treat abnormal movement. The severity of the tardive dystonia and dyskinesia was evaluated using the Abnormal Involuntary Movement Scale (AIMS) before and after the course of ECT. The patients who displayed a greater than 50% improvement in the AIMS score were classified as the responders. Results The mean AIMS score decreased from 19.1±4.7 to 9.6±4.2. There were seven responders among the 18 patients, which yielded a 39% response rate. Conclusion ECT has a moderate but significant effect on tardive dystonia and dyskinesia.
    Neuropsychiatric Disease and Treatment 07/2014; 10:1209-12. DOI:10.2147/NDT.S62490 · 1.74 Impact Factor
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    • "Vitamin E, which neutralizes free radicals, has been investigated in multiple studies. Although a large multicenter study showed minimal acute benefit on reducing abnormal motor movements,86–88 vitamin E may have more significant benefit at protecting against the deterioration of TDK symptoms over time.89 Melatonin, another antioxidant, was found to be effective in one randomized controlled trial.90 "
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    ABSTRACT: Tardive dyskinesia (TDK) includes orobuccolingual movements and "piano-playing" movements of the limbs. It is a movement disorder of delayed onset that can occur in the setting of neuroleptic treatment as well as in other diseases and following treatment with other drugs. The specific pathophysiology resulting in TDK is still not completely understood but possible mechanisms include postsynaptic dopamine receptor hypersensitivity, abnormalities of striatal gamma-aminobutyric acid (GABA) neurons, and degeneration of striatal cholinergic interneurons. More recently, the theory of synaptic plasticity has been proposed. Considering these proposed mechanisms of disease, therapeutic interventions have attempted to manipulate dopamine, GABA, acetylcholine, norepinephrine and serotonin pathways and receptors. The data for the effectiveness of each class of drugs and the side effects were considered in turn.
    Neuropsychiatric Disease and Treatment 09/2013; 9:1371-1380. DOI:10.2147/NDT.S30767 · 1.74 Impact Factor
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