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Author Notes:

Stewart A. Factor, Email: sfactor@emory.edu

The author would like to thank Rachel H. Factor, PharmD, and Laura M. Scorr, MD, for their careful review and constructive comments.

Dr. Factor has the following disclosures: honoraria: Lundbeck, Sunovion, Biogen, Acadia, Impel, Acorda, and CereSpir; grants: Medtronics, Boston Scientific, Biohaven, Impax, Lilly, US World Meds, Sunovion Therapeutics, Vaccinex, Voyager, Jazz Pharmaceuticals, Cure Huntington's Disease Initiative Foundation, Michael J. Fox Foundation, National Institutes of Health (U10 NS077366), and Parkinson Foundation; and royalties: Demos, Blackwell Futura, Springer for textbooks, Uptodate, Other Bracket Global Limited Liability Company, and Clinical Neuroscience Solutions Ratings Limited Liability Company.


Research Funding:

The study received funding from Sartain Lanier Family Foundation.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Clinical Neurology
  • Neurosciences
  • Pharmacology & Pharmacy
  • Neurosciences & Neurology
  • Tardive syndrome
  • therapy
  • VMAT2 inhibitors
  • deep brain stimulation
  • botulinum toxin

Management of Tardive Syndrome: Medications and Surgical Treatments


Journal Title:



Volume 17, Number 4


, Pages 1694-1712

Type of Work:

Article | Final Publisher PDF


Tardive syndrome (TS) is an iatrogenic, often persistent movement disorder caused by drugs that block dopamine receptors. It has a broad phenotype including movement (orobuccolingual stereotypy, dystonia, tics, and others) and nonmotor features (akathisia and pain). TS has garnered increased attention of late because of the Food and Drug Administration approval of the first therapeutic agents developed specifically for this purpose. This paper will begin with a discussion on pathogenesis, clinical features, and epidemiology. However, the main focus will be treatment options currently available for TS including a suggested algorithm based on current evidence. Recently, there have been significant advances in TS therapy, particularly with the development of 2 new vesicular monoamine transporter type 2 inhibitors for TS and with new data on the efficacy of deep brain stimulation. The discussion will start with switching antipsychotics and the use of clozapine monotherapy which, despite the lack of higher-level evidence, should be considered for the treatment of psychosis and TS. Anti-dyskinetic drugs are separated into 3 tiers: 1) vesicular monoamine transporter type 2 inhibitors, which have level A evidence, are approved for use in TS and are recommended first-choice agents; 2) drugs with lower level of evidence for efficacy including clonazepam, Ginkgo biloba, and amantadine; and 3) drugs that have the potential to be beneficial, but currently have insufficient evidence including levetiracetam, piracetam, vitamin B6, melatonin, baclofen, propranolol, zolpidem, and zonisamide. Finally, the roles of botulinum toxin and surgical therapy will be examined. Current therapies, though improved, are symptomatic. Next steps should focus on the prevention and reversal of the pathogenic process.

Copyright information:

© The American Society for Experimental NeuroTherapeutics, Inc. 2020

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/rdf).
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