Pharmacological treatment of tardive dyskinesia: recent developments

ABSTRACT

Introduction: Tardive dyskinesia (TD) occurs in patients receiving antipsychotic treatment with dopamine receptor antagonists. Despite the prevalence of TD and its negative impact on patients’ lives, there has been a lack of approved treatments and limited evidence from controlled trials of pharmacological treatment.

Areas covered: PubMed was searched for English-language papers published during 2007–2016 using terms ‘tardive dyskinesia’ or ‘drug-induced movement disorder’, and ‘treatment’. Studies evaluating pharmacological agents for the treatment of TD were selected. A total of 26 studies (five meta-analyses, twelve randomized controlled trials, and nine open-label observational studies) are reviewed.

Expert commentary: Treatment of TD necessitates a stepwise approach. Optimization of antipsychotic therapy should be considered before initiation of antidyskinetic therapies. Data from some recent studies indicate possible improvements in TD after switching antipsychotics or with the use of amantadine, levetiracetam, piracetam, zonisamide, propranolol, vitamin B₆, or certain unregulated herbal medicines; although significance of these improvements is unclear and require further investigation in randomized controlled trials. By contrast, recent evidence from Phase III trials of novel vesicular monoamine transporter-2 inhibitors demonstrates they could have a significant effect on TD symptom severity and suggests these agents may have the potential to transform treatment of TD in coming years.

KEYWORDS:

• Antidyskinetic
• antipsychotic
• supplement
• tardive dyskinesia
• treatment

Acknowledgments

The systematic literature search was conducted by Holly Trautman (HT) and Jamie Dunning (JD) of Aventine Consulting LLC, funded by Teva Pharmaceuticals. Editorial assistance in the development of the manuscript was provided by Dr Kirsteen Munn of Anthemis Consulting Ltd, funded by Teva Pharmaceuticals

Declaration of interest

SN Caroff is a consultant for Teva Pharmaceutical Industries and Neurocrine Biosciences. B Carroll is an employee of Teva Pharmaceutical Industries. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Additional information

Funding

This paper was funded by Teva Pharmaceuticals.