Tardive dyskinesia is a disfiguring and disabling disorder of voluntary control of movement, often caused by antipsychotic drugs. Several Cochrane reviews have summarised the effects of the many treatments used to manage these involuntary movements. This review summarises the trial-based evidence of a miscellaneous group of compounds (botulin toxin, endorphin, essential fatty acid, EX11582A, ganglioside, insulin, lithium, naloxone, oestrogen, periactin, phenylalanine, piracetam, stepholidine, tryptophan, neurosurgery, or ECT) none of which were found to be effective for tardive dyskinesia.
There is no strong evidence to support the everyday use of any of the agents included in this review. All results must be considered inconclusive and these compounds probably should only be used within the context of a well-designed evaluative study.
Tardive dyskinesia is a disabling movement disorder associated with the prolonged use of neuroleptic medication. This review, one in a series examining the treatment of tardive dyskinesia, will cover miscellaneous treatments not covered elsewhere.
To determine whether the following interventions were effective and safe for people with neuroleptic induced tardive dyskinesia: botulin toxin, endorphin, essential fatty acid, EX11582A, ganglioside, insulin, lithium, naloxone, oestrogen, periactin, phenylalanine, piracetam, stepholidine, tryptophan, neurosurgery, or ECT.
For the current update of this review (September 2009) we searched the Cochrane Schizophrenia Group Trials Register which is based on regular searches of CINAHL, EMBASE, MEDLINE and PsycINFO.
Studies were selected if they focused on people with schizophrenia or other chronic mental illnesses with neuroleptic-induced tardive dyskinesia, and compared the use of the interventions listed above versus placebo or no intervention.
We reliably selected, quality assessed and data extracted studies. Data were excluded where more than 50% of participants in any group were lost to follow up. For binary outcomes we used a fixed effects risk ratio (RR) and its 95% confidence interval (CI) was calculated. Where possible, the weighted number needed to treat/harm statistic (NNT/H), and its 95% confidence interval (CI), were also calculated. For continuous outcomes, endpoint data were preferred to change data. Non-skewed data from valid scales were to have been synthesised using a weighted mean difference (WMD).
We included nine studies. Ceruletide is not clearly more effective than placebo (n=132, 2 RCTs, RR not any improvement in tardive dyskinesia 0.83 CI 0.7 to 1.1). This also applied to gamma-linolenic acid, although data were sparse (n=16, 1 RCT, RR no clinical improvement 1.00 CI 0.7 to 1.5), oestrogen (n=12, 1 RCT, RR no clinically important improvement 1.2 CI 0.8 to 1.8), and lithium (n=11, 1 RCT, RR no clinically important improvement 1.39 CI 0.6 to 3.1). Phenylalanine may even be detrimental (n=18, 1 RCT, MD AIMS score 4.40 CI 1.2 to 7.6). In one small study we found that insulin is more likely to produce a clinical improvement in tardive dyskinesia than placebo (n=20, 1 RCT, RR no clinical improvement 0.52 CI 0.3 to 1.0, NNT 2 CI 1 to 5). In another small study we found tardive dyskinesia scores favoured the control group given placebo compared with those given piracetam (n=35, 1 RCT, MD 2.60 CI 2.0 to 3.3). The number of participants leaving the study early favoured participants given eicosapentaenoic acid (n=84, 1 RCT, RR 0.39 CI 0.2 to 0.7, NNT 3 CI 3 to 8) compared with the placebo group.