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Pharmacological interventions
Vesicular monoamine transporter type 2 inhibition can lead to effective and tolerable management of tardive dyskinesia
  1. Leslie Citrome
  1. Correspondence to Psychiatry and Behavioral Sciences, New York Medical College, Valhalla, NY 10595, USA; citrome{at}cnsconsultant.com

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Commentary on: Anderson KE, Stamler D, Davis MD, et al. Deutetrabenazine for treatment of involuntary movements in patients with tardive dyskinesia (AIM-TD): a double-blind, randomised, placebo-controlled, phase 3 trial. Lancet Psychiatry. 2017 Aug;4(8):595–604.

What is already known on this topic  

Tardive dyskinesia (TD), characterised by involuntary movements of the tongue, lips, face, trunk and extremities, is thought to be a generally irreversible consequence of the use of dopamine receptor blocking agents and is not rare. The introduction of second-generation antipsychotics has not  eliminated TD. Vesicular monoamine transporter type 2 (VMAT2) inhibition has been known to reduce TD, as observed with tetrabenazine, but tetrabenazine has been relatively complex to use because of its short half-life and sensitivity to CYP2D6 metabolism.1 Deutetrabenazine is related to tetrabenazine in that deuterium is substituted for hydrogen at the key sites of primary metabolism, altering the pharmacokinetics of drug metabolism by slowing it down.

Methods of the study

In this randomised, double-blind, placebo-controlled study, …

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