Tardive dyskinesia

Olga Waln MD (Dr Waln of Houston Methodist Neurological Institute has no relevant financial relationships to disclose.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released November 23, 1993; last updated February 27, 2017; expires February 27, 2020

Overview

Tardive dyskinesia is a group of delayed-onset iatrogenic movement disorders caused by dopamine receptor-blocking medications that can manifest as orobuccolingual stereotypy, dystonia, akathisia, tics, tremor, chorea, or as a combination of different involuntary movements. Abnormal movements can persist for years despite discontinuation of the offending drug. In many cases, tardive dyskinesia can be an irreversible condition, resistant to pharmacological treatment. Awareness of offending agents and early recognition of tardive dyskinesia is, therefore, important in clinical practice. This article presents an overview of the etiology, pathophysiology, phenomenology, and treatment of tardive dyskinesia.

Key points

 

• Tardive dyskinesia usually occurs after prolonged exposure to medications with dopamine receptor-blocking properties and may emerge during the course of treatment or following discontinuation of the medication or reduction of the dose.

 

• Patients more vulnerable to developing tardive dyskinesia are older women and patients with previous brain damage, preexisting drug-induced parkinsonism, and greater total drug exposure.

 

• Tardive dyskinesia may not improve, despite discontinuation of the offending agent.

 

• The pathophysiology of tardive dyskinesia remains poorly understood.

 

• There are many potential treatment strategies for tardive dyskinesia, but at this time, there are no standard and established treatments.

Historical note and terminology

Neuroleptics were introduced in 1952 for treatment the of schizophrenia, and the first case of drug-induced orofacial-lingual stereotypy, referred to as “paroxysmal dyskinesia,” was reported 5 years later (Schonecker 1957). Unlike acute drug-induced movement disorders (acute dystonic reaction) or dose-dependent reversible conditions (drug-induced parkinsonism) that subside with discontinuation of the medication, other hyperkinetic movement disorders can have delayed onset for months or years after the initial dose, hence, the name “tardive.” The term "tardive dyskinesia" was first introduced in 1964 and is now commonly used to identify any tardive movement disorder, including stereotypy, akathisia, dystonia, myoclonus, tics, chorea, and tremor (Faurbye et al 1964). Frequently, however, clinicians reserve the term “tardive dyskinesia” or “classic tardive dyskinesia” when referring to orofacial-lingual stereotypy, and they use the term “tardive syndrome” for all tardive movement disorders, especially those cases manifesting as a combination of a few different abnormal movements. The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-V), defines tardive dyskinesia as “involuntary athetoid or choreiform movements lasting at least a few weeks, developing in association with the use of a neuroleptic medication for at least a few months, and persisting beyond 4-8 weeks” (American Psychiatric Association 2013). However, this definition fails to identify other nonneuroleptic agents that can cause tardive dyskinesia, or to include all phenomenological presentations of tardive syndrome.

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