Progress in Neuro-Psychopharmacology and Biological Psychiatry
Botulinum toxin in the treatment of orofacial tardive dyskinesia: A single blind study
Introduction
Tardive dyskinesia (TD) is a serious, potentially irreversible side effect and its average prevalence in patients on long term antipsychotic treatment with first generation antipsychotics can be estimated around 30% (Jankovic, 1995). Most frequent is the orofacial form of tardive dyskinesia (OTD), accounting for approximately 80% of TD cases (Rapaport et al., 2000). OTD may cause physical problems such as disturbances in speech articulation and eating. It often leads to psychological distress. There are only a few albeit restricted approaches to treat TD, such as L-dopa, tiapride, vitamin E (Soares and McGrath, 1999). The efficacy of Botulinum Toxin A (BTA) in dystonia is well established (Costa et al., 2005a, Costa et al., 2005b). Based on several case reports and one open clinical trial, BTA may also be effective in the treatment of OTD (Rapaport et al., 2000, Truong et al., 1990, Yasufuku-Takano et al., 1995, Van Harten and Hovestadt, 2006). Therefore, we conducted a single blind study to evaluate the hypothesis that botulinum toxin can reduce the severity of OTD.
Section snippets
Methods
Clinicians treating chronically mentally ill patients at the Parnassia Psychiatric Institute in The Hague were asked to refer patients with orofacial tardive dyskinesia for the study.
Results
Of the 15 patients referred to the study, 12 (8 males and 4 females) with a mean age of 51 years (S.D. 8.8 and range 34–60 years) fulfilled the inclusion criteria. Table 1 shows demographic and clinical data. Diagnostically eight patients had schizophrenia, one schizoaffective disorder, one bipolar disorder, one an organic psychosyndrome and one mental retardation. The mean total dosage of the third treatment session was 72.8 Mu (range 40–80). The inter-rate reliability of the 2 blind raters of
Discussion
This first single blind study of Botulinium Toxin A as a treatment for orofacial tardive dyskinesia showed a non-significant tendency for improvement in the group as a whole. Given the long duration of the study (> 8 months) and the severity of the population, psychotic relapses were likely to happen, prompting inevitable adjustments of the psychotropic medication. As changing antipsychotic dosage may have influenced TD severity, this could have biased the effect of the BTA in four patients.
Conclusion
In conclusion, BTA was well tolerated, whereas the results of its efficacy on OTD were inconclusive. However, given the severity of TD as a clinical problem and the scarcity of efficacious treatments available to date, the therapeutic potential of BTA should be further explored, adequately dosed in a double blind placebo-controlled study design.
Acknowledgments
This study was supported by the Stichting tot Steun VCVGZ, Arnhem, the Netherlands.
The BTA ampules were purchased from Ipsen, Porton, United Kingdom.
The results of this study were presented in part at the Schizophrenia Winter Workshop at Davos, February 2006.
We would like to thank Majid Aramideh, Huib Burger, Tonko Hoffman, Hans Oolders and Cokky van der Venne for their clinical and statistical support.
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