Last updated:
07/16/2025
Years published: 1987, 1989, 1995, 1998, 1999, 2007, 2009, 2012, 2015, 2018, 2025
NORD gratefully acknowledges Gioconda Alyea, MD (FMG), MS, National Organization for Rare Disorders and Daniel Tarsy, MD, Professor in Neurology, Harvard Medical School; Director, Parkinson’s Disease & Movement Disorders Center, Beth Israel Deaconess Medical Center, for assistance in the preparation of this report.
Summary
Tardive dyskinesia (TD) is an involuntary neurological movement disorder caused by taking dopamine receptor blocking drugs that are prescribed to treat certain psychiatric or gastrointestinal conditions. Long-term use of these drugs may produce biochemical abnormalities in the area of the brain known as the striatum in the basal ganglia.
The reasons that some people who take these drugs get tardive dyskinesia and some people do not, is unknown. Tardive dystonia is a more severe form of tardive dyskinesia in which slower twisting movements of the neck and trunk muscles are prominent.
Treatment includes stopping or reducing the medication that triggered TD and specific medications to improve the symptoms.
Introduction
Tardive dyskinesia does not meet the definition of a rare disease in the U.S. (fewer than 200,000 Americans). NORD posts this report because limited information is available about this condition, and it may be underdiagnosed.
Tardive dyskinesia is characterized by involuntary and abnormal movements of the jaw, lips and tongue. Typical symptoms include facial grimacing, sticking out the tongue and sucking or fish-like movements of the mouth. In some people, the arms and/or legs may also be affected by involuntary rapid, jerking movements (chorea), or slow, writhing movements (athetosis). Symptoms of tardive dystonia include slower, twisting movements of larger muscles of the neck and trunk as well as the face.
Tardive dyskinesia (TD) is most commonly associated with the long-term use of a group of medications known as dopamine receptor blocking agents (DRBAs). These medications are frequently prescribed to treat psychiatric conditions like schizophrenia and bipolar disorder, as well as certain gastrointestinal and neurological problems.
Dopamine is a chemical messenger in the brain, called a neurotransmitter, that plays a vital role in controlling mood, movement and thought processes. DRBAs work by blocking dopamine receptors, particularly a subtype called D2 receptors, which help reduce symptoms of psychosis such as hallucinations and delusions. There are two main types of antipsychotics, first-generation (also called typical antipsychotics), which strongly block D2 receptors and second-generation (atypical antipsychotics), which have a weaker effect on these receptors and act on other brain chemicals like serotonin. While second-generation antipsychotics may carry a lower risk, they can still increase the risk of developing TD, especially in older adults or people who take these medications over a long period.
The underlying causes of TD are complex. One major factor is the brain’s response to prolonged dopamine receptor blockade. Over time, the brain may become overly sensitive to dopamine, a process known as receptor hypersensitivity which can lead to involuntary movements seen in TD. Additionally, research shows that oxidative stress, an imbalance between harmful molecules called reactive oxygen species and the body’s ability to detoxify them, may damage brain cells and contribute to TD. Chronic use of dopamine-blocking medications can increase this stress, particularly in a part of the brain called the basal ganglia, which helps control movement.
It is not known why some people who use these medications develop TD and others do not.
Some people may be more likely to develop TD due to inherited changes in how their bodies process medications or regulate brain chemistry. Scientists have identified changes (variants) in certain genes, such as those related to dopamine receptors and the body’s antioxidant defenses, that may increase a person’s vulnerability. Other brain systems, including those that use gamma-aminobutyric acid (GABA) and glutamate, two important neurotransmitters involved in regulating brain activity, are also being studied for their possible involvement.
Although TD most often appears after years of medication use, it can also develop after a shorter time in some people. Other dopamine-blocking medications like metoclopramide and prochlorperazine, which are sometimes used to treat long-term digestive issues, have also been linked to TD.
Research suggests that at least one in five people (20%) who take first-generation antipsychotic medications may develop tardive dyskinesia. Other drugs can also cause this condition, but studies are more limited. Available reports estimate that between 1% and 10% of people who take them may be affected with TD. The prevalence (number of people diagnosed) with TD in 2016 was estimated to be 573,000 which is about 9% of people who take antipsychotic medications. A high percentage of people with schizophrenia who have taken these drugs for a long period of time have a high risk of developing TD.
Treatment
The American Academy of Neurology (AAN) guidelines emphasize that managing tardive dyskinesia (TD) begins with early recognition of involuntary facial, neck, trunk, or limb movements in anyone taking neuroleptic (antipsychotic) medications. When such movements appear, safely discontinuing the drug or reducing the dose is the first step, provided this can be done without jeopardizing psychiatric stability. Often, an atypical (second-generation) antipsychotic is substituted for a traditional, first-generation drug; however, it’s important to know that these newer drugs can also trigger or perpetuate TD. In some people, if symptoms worsen markedly after stopping treatment, it may be necessary to restart the medication.
Alongside careful medication adjustments, the AAN strongly recommends the use of the VMAT2 inhibitors valbenazine and deutetrabenazine, to directly target and reduce abnormal movements.
Valbenazine (Ingrezza) was approved by the U.S. Food and Drug Administration (FDA) in 2017 to treat TD and the sprinkle formulation (Ingrezza Sprinkle) was approved by the FDA in 2024.
Deutetrabenazine (Austedo) was also FDA approved to treat TD in 2017 and the extended-release version (Austedo XR) was FDA approved in 2023.
These medications have been shown in clinical trials to lessen the severity of TD and are considered the first option of treatment once symptoms are established.
Clozapine remains an important alternative for some people, as its lower propensity to cause TD can both protect against new movements and, in some people, improve existing symptoms.
Other medications such as ginkgo biloba or amantadine may be considered when standard treatments are insufficient, though the supporting data is more limited.
In addition, behavioral therapy and counseling can be very useful in addressing the emotional and social challenges that often accompany TD. Because long-term use of dopamine-blocking medications has an ongoing risk, regular monitoring for early signs of TD is essential. Open communication among patients, caregivers and doctors, sharing concerns, discussing risks and benefits, and reporting any new or worsening movements promptly ensures timely intervention and the best possible quality of life.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Tollfree: (800) 411-1222
TTY: (866) 411-1010
Email: [email protected]
Some current clinical trials also are posted on the following page on the NORD website:
https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/
For information about clinical trials sponsored by private sources, contact:
www.centerwatch.com
For information about clinical trials conducted in Europe, contact:
https://www.clinicaltrialsregister.eu/
JOURNAL ARTICLES
North CS, McDonald K, Hunter J, et al. Prevalence of tardive dyskinesia in an electronic medical record study at a large community mental health treatment center. Prim Care Companion CNS Disord. 2022;24(4):21m03069. https://doi.org/10.4088/PCC.21m03069
Dhir A, Schilling T, Abler V, Potluri R and Carroll B. Estimation of epidemiology of tardive dyskinesia in the United States (P2.018). Neurology. 2017; 88(16_supplement). https://www.neurology.org/doi/10.1212/WNL.88.16_supplement.P2.018
INTERNET
Online Mendelian Inheritance in Man (OMIM). Johns Hopkins University, Last update 03/31/2009. Entry Number 272620. Available at: https://omim.org/entry/272620 Accessed July 10, 2025.
Vasan S, Padhy RK. Tardive Dyskinesia. [Updated 2023 Apr 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448207/ Accessed July 10, 2025.
Brasic JR. Tardive Dyskinesia Guidelines. Medscape Reference. August 19, 2024. Available at: https://emedicine.medscape.com/article/1151826-guidelines Accessed July 10, 2025.
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