URL of this page: //medlineplus.gov/ency/article/000685.htm
Tardive dyskinesia (TD) is a disorder that involves involuntary movements. Tardive means delayed and dyskinesia means abnormal movement.
TD is a serious side effect that occurs when you take medicines called neuroleptics. These drugs are also called antipsychotics or major tranquilizers. They are used to treat mental problems.
TD often occurs when you take the drug for many months or years. In some cases, it occurs after you take them for as little as 6 weeks.
Medicines that most commonly cause this disorder are older antipsychotics, including:
Newer antipsychotics seem less likely to cause TD, but they are not entirely without risk.
Other drugs that can cause TD include:
- Metoclopramide (treats stomach problem called gastroparesis )
- Antidepressant drugs such as amitriptyline, fluoxetine, phenelzine, sertraline, trazodone
- Antiparkinson drugs such as levodopa
- Antiseizure drugs such as phenobarbital and phenytoin
Symptoms of TD include uncontrollable movements of the face and body such as:
- Facial grimacing (commonly involving lower facial muscles)
- Finger movement (piano playing movements)
- Rocking or thrusting of the pelvis (duck-like gait)
- Jaw swinging
- Repetitive chewing
- Rapid eye blinking
- Tongue thrusting
When TD is diagnosed, the health care provider will either have you stop the medicine slowly or switch to another one.
If TD is mild or moderate, various medicines may be tried. A dopamine-depleting medicine, tetrabenazine is most effective treatment for TD. Your provider can tell you more about these.
If TD is very severe, a procedure called deep brain stimulation DBS may be tried. DBS uses a device called a neurostimulator to deliver electrical signals to the areas of the brain that control movement.
If diagnosed early, TD may be reversed by stopping the medicine that caused the symptoms. Even if the medicine is stopped, the involuntary movements may become permanent, and in some cases, may become worse.
TD; Tardive syndrome; Orofacial dyskinesia; Involuntary movement – tardive dyskinesia; Antipsychotic drugs – tardive dyskinesia; Neuroleptic drugs – tardive dyskinesia; Schizophrenia – tardive dyskinesia
- Central nervous system and peripheral nervous system
Aronson JK. Neuroleptic drugs. In: Aronson JK, ed. Meyler’s Side Effects of Drugs. 16th ed. Waltham, MA: Elsevier B.V.; 2016:chap 53.
Freudenreich O, Flaherty AW. Patients with abnormal movements. In: Stern TA, Freudenreich O, Smith FA, Fricchione GL, Rosenbaum JF, eds. Massachusetts General Hospital Handbook of General Hospital Psychiatry. 7th ed. Philadelphia, PA: Elsevier; 2017:chap 21.
Freudenreich O, Goff DC, Henderson DC. Antipsychotic drugs. In: Stern TA, Fava M, Wilens TE, Rosenbaum JF, eds. Massachusetts General Hospital Comprehensive Clinical Psychiatry. 2nd ed. Philadelphia, PA: Elsevier; 2016:chap 42.
Lang AE. Other movement disorders. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 410.
Review Date 4/30/2018
Updated by: Amit M. Shelat, DO, FACP, Attending Neurologist and Assistant Professor of Clinical Neurology, SUNY Stony Brook, School of Medicine, Stony Brook, NY. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.
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Definition of tardive dyskinesia
: a neurological disorder characterized by involuntary uncontrollable movements especially of the mouth, tongue, trunk, and limbs and occurring especially as a side effect of prolonged use of antipsychotic drugs (such as phenothiazine)
Examples of tardive dyskinesia in a Sentence
Recent Examples on the Web
Antipsychotics may also cause side effects such as tardive dyskinesia (a disorder that induces repetitive and involuntary movements), although newer ones generally come with fewer serious side reactions, the Mayo Clinic notes.
Nina Bahadur, SELF, “9 Facts to Know About Schizophrenia, Which Is Way Too Misunderstood,” 15 Sep. 2018
And yet, in high doses and over the long term, patients often experienced tardive dyskinesia, which includes tongue thrusting, lip smacking, restlessness, involuntary movements of arms and legs, which become twisted like pretzels.
Maggie Jones, New York Times, “A Reckoning With an Imperfect Science in ‘Blue Dreams’,” 3 Apr. 2018
Was told by psychiatrists for 10 years that 100 mg Seroquel would never cause tardive dyskinesia [a severe movement disorder.] . .
Amy Ellis Nutt, Washington Post, “One of America’s most popular drugs — first aimed at schizophrenia — reveals the issues of ‘off-label’ use,” 30 Mar. 2018
These example sentences are selected automatically from various online news sources to reflect current usage of the word ‘tardive dyskinesia.’ Views expressed in the examples do not represent the opinion of Merriam-Webster or its editors. Send us feedback .
First Known Use of tardive dyskinesia
1964, in the meaning defined above
History and Etymology for tardive dyskinesia
tardive tending toward late development (from French, feminine of tardif, from Middle French) + dyskinesia
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Medical Definition of tardive dyskinesia
: a neurological disorder characterized by involuntary uncontrollable movements especially of the mouth, tongue, trunk, and limbs and occurring especially as a side effect of prolonged use of antipsychotic drugs (as phenothiazine)
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|Synonyms||Linguofacial dyskinesia, tardive dystonia, tardive oral dyskinesia |
|Tardive dyskinesia is believed to involve the neurotransmitter dopamine .|
|Specialty||Neurology , psychiatry|
|Symptoms||Involuntary, repetitive body movements |
|Causes||Neuroleptic medications (antipsychotics, metoclopramide )  |
|Diagnostic method||Based on symptoms after ruling out other potential causes |
|Differential diagnosis||Huntington’s disease , cerebral palsy , Tourette syndrome , dystonia |
|Prevention||Using lowest possible dose of neuroleptic medication |
|Treatment||Stopping neuroleptic medication if possible, switching to clozapine |
|Medication||Valbenazine , tetrabenazine , botulinum toxin  |
|Frequency||20% (atypical antipsychotics) 30% (typical antipsychotics) |
Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements.  This may include grimacing, sticking out the tongue, or smacking the lips.  Additionally there may be rapid jerking movements or slow writhing movements .  In about 20% of people, decreased functioning results. 
Tardive dyskinesia occurs in some people as a result of long-term use of neuroleptic medications (antipsychotics, metoclopramide ).   These medications are usually used for mental illness , but may also be given for gastrointestinal or neurological problems.  The condition typically develops only after months to years of use.   The diagnosis is based on the symptoms after ruling out other potential causes. 
Efforts to prevent the condition include not using or using the lowest possible dose of neuroleptics.  Treatment includes stopping the neuroleptic medication if possible or switching to clozapine .  Other medications such as valbenazine , tetrabenazine , or botulinum toxin may be used to lessen the symptoms.   With treatment some see a resolution of symptoms while others do not. 
Rates in those on atypical antipsychotics are about 20%, while those on typical antipsychotics have rates of about 30%.  Risk is greater in older people.  The term “tardive dyskinesia” first came into use in 1964. 
- 1 Signs and symptoms
- 2 Causes
- 2.1 Risk factors
- 3 Prevention
- 4 Treatment
- 5 Epidemiology
- 6 References
- 7 External links
Signs and symptoms[ edit ]
Tardive dyskinesia is characterized by repetitive, involuntary movements. Some examples of these types of involuntary movements include: 
- Tongue movements
- Lip smacking
- Lip puckering
- Pursing of the lips
- Excessive eye blinking
Rapid, involuntary movements of the limbs, torso, and fingers may also occur.  In some cases, an individual’s legs can be so affected that walking becomes difficult or impossible.  These symptoms are the opposite of patients who are diagnosed with Parkinson’s disease . Parkinson’s patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving. 
Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the prevalence rate is relatively low. 
Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder ,  and as a result patients are prescribed neuroleptic drugs, which increase the probability that the patient will develop a severe and disabling case, and shortening the typical survival period. 
Other closely related neurological disorders have been recognized as variants of tardive dyskinesia. Tardive dystonia is similar to standard dystonia but permanent. Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body. In some extreme cases, afflicted individuals experience so much internal torture that they lose their ability to sit still. Tardive tourettism is a tic disorder featuring the same symptoms as Tourette syndrome . The two disorders are extremely close in nature and often can only be differentiated by the details of their respective onsets. Tardive myoclonus , a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities. 
“AIMS Examination”: This test is used when psychotropic medications have been prescribed because patients sometimes develop tardive dyskinesia due to prolonged use of antipsychotic medications. The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD). The test is not meant to tell whether there is an absence or presence of tardive dyskinesia. It just scales to level of symptoms indicated by the actions observed. The levels range from none to severe. The AIMS examination was constructed in the 1970s to measure involuntary facial, trunk, and limb movements. It is best to do this test before and after the administration of the psychotropic drugs. Taking the AIMS consistently can help to track severity of TD over time.  
Causes[ edit ]
Tardive dyskinesia was first described in the 1950s shortly after the introduction of chlorpromazine and other antipsychotic drugs .  However, the exact mechanism of the disorder remains largely uncertain. The most compelling line of evidence suggests that tardive dyskinesia may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway , with the D2 dopamine receptor being most affected. Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia.  The D2 hypersensitivity hypothesis is also supported by evidence of a dose-response relationship, withdrawal effects, studies on D2 agonists and antagonists, animal studies, and genetic polymorphism research. 
Given similar doses of the same neuroleptic, differences among individuals still exist in the likelihood of developing tardive dyskinesia. Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins. Decreased functional reserve or cognitive dysfunction, associated with aging, mental retardation, alcohol and drug abuse, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics.  Antipsychotic drugs can sometimes camouflage the signs of tardive dyskinesia from occurring in the early stages; this can happen from the individual having an increased dose of an antipsychotic drug. Often the symptoms of tardive dyskinesia are not apparent until the individual comes off of the antipsychotic drugs; however, when tardive dyskinesia worsens, the signs become visible. 
Other dopamine antagonists and antiemetics can cause tardive dyskinesia, such as metoclopramide and promethazine , used to treat gastrointestinal disorders . Atypical antipsychotics are considered lower-risk for causing TD than their typical counterparts with their relative rates of TD of 13.1% and 32.4% respectively in short-term trials with haloperidol being the main typical antipsychotic utilised in said trials.  Quetiapine and clozapine are considered the lowest risk agents for precipitating TD.  From 2008, there have been reported cases of the anti-psychotic medication aripiprazole , a partial agonist at D2 receptors, leading to tardive dyskinesia. 
As of 2013, reports of tardive dyskinesia in aripiprazole have grown in number. 
The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the patient more sensitive to tardive dyskinesia. Since 1973 the use of these drugs has been found to be associated with the development of tardive dyskinesia.  
Risk factors[ edit ]
An increased risk of tardive dyskinesia has been associated with smoking in some studies,   although a negative study does exist.  There seems to be a cigarette smoke-exposure-dependent risk for TD in antipsychotic-treated patients.  Elderly patients are also at a heightened risk for developing TD,  as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia.  TD is also more common in those that experience acute neurological side effects from antipsychotic drug treatment.  Racial discrepancies in TD rate also exist, with Africans and African Americans having higher rates of TD after exposure to antipsychotics.  Certain genetic risk factors for TD have been identified including polymorphisms in the genes encoding the D3 , 5-HT2A and 5-HT2C receptors. 
Prevention[ edit ]
Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. However, with diseases of chronic psychosis such as schizophrenia, this strategy must be balanced with the fact that increased dosages of neuroleptics are more beneficial in preventing recurrence of psychosis. If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal of the drug for months, years or even permanently.   Some studies suggest that physicians should consider using atypical antipsychotics as a substitute to typical antipsychotics for patients requiring medication. These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia. 
Studies have tested the use of melatonin , high dosage vitamins , and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia ) as a way of preventing and treating tardive dyskinesia. Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current prevalence rate for those taking antipsychotic drugs.  Tentative evidence supports the use of vitamin E for prevention. 
Treatment[ edit ]
Valbenazine was approved by the FDA for tardive dyskinesia in April 2017.  Tetrabenazine , which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders (e.g. Huntington’s chorea).  Deutetrabenazine , an isotopic isomer of tetrabenazine, was approved by the FDA for tardive dyskinesia in August 2017.  Vitamin B6 has been reported to be an effective treatment for TD in two randomised double-blind placebo-controlled trials,   but the overall evidence for its effectiveness is considered “weak.”  Clonidine may also be useful in the treatment of TD, although dose-limiting hypotension and sedation may hinder its usage.  Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia.  As of 2018 evidence is insufficient to support the use of benzodiazepines , baclofen , progabide , sodium valproate , tetrahydroisoxazolopyridinol , or calcium channel blockers (e.g. diltiazem ).   
Epidemiology[ edit ]
Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. The average prevalence rate has been estimated to be around 30% for individuals taking antipsychotic medication, such as that used to treat schizophrenia.  A study being conducted at the Yale University School of Medicine has estimated that “32% of patients develop persistent tics after 5 years on major tranquilizers, 57% by 15 years, and 68% by 25 years.”  More drastic data was found during a longitudinal study conducted on individuals 45 years of age and older who were taking antipsychotic drugs. According to this research study, 26% of patients developed tardive dyskinesia after just one year on the medication. Another 60% of this at-risk group developed the disorder after 3 years, and 23% developed severe cases of tardive dyskinesia within 3 years.  According to these estimates, the majority of patients will eventually develop the disorder if they remain on the drugs long enough. 
Elderly patients are more prone to develop tardive dyskinesia, and elderly women are more at-risk than elderly men. The risk is much lower for younger men and women, and also more equal across the sexes.  Patients who have undergone electroconvulsive therapy or have a history of diabetes or alcohol abuse also have a higher risk of developing tardive dyskinesia. 
Several studies have recently been conducted comparing the prevalence rate of tardive dyskinesia with second generation, or more modern, antipsychotic drugs to that of first generation drugs. The newer antipsychotics appear to have a substantially reduced potential for causing tardive dyskinesia. However, some studies express concern that the prevalence rate has decreased far less than expected, cautioning against the overestimation of the safety of modern antipsychotics.  
A physician can evaluate and diagnose a patient with tardive dyskinesia by conducting a systematic examination. The physician should ask the patient to relax, and look for symptoms like facial grimacing, eye or lip movements, tics, respiratory irregularities, and tongue movements. In some cases, patients experience nutritional problems, so a physician can also look for a gain or loss in weight. 
Apart from the underlying psychiatric disorder, tardive dyskinesia may cause afflicted people to become socially isolated. It also increases the risk of body dysmorphic disorder (BDD) and can even lead to suicide. Emotional or physical stress can increase the severity of dyskinetic movements, whereas relaxation and sedation have the opposite effect. 
References[ edit ]
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- ^ Llorca, Pierre-Michel; Chereau, Isabelle; Bayle, Frank-Jean; et al. (2002). “Tardive dyskinesias and antipsychotics: A review”. European Psychiatry. 17 (3): 129–38. doi : 10.1016/S0924-9338(02)00647-8 . PMID 12052573 .
- ^ Glenmullen, Joseph (2001). Prozac Backlash: Overcoming the Dangers of Prozac, Zoloft, Paxil, and Other Antidepressants With Safe, Effective Alternatives. New York: Simon & Schuster. p. 38. ISBN 978-0-7432-0062-2 .[ unreliable medical source? ] ::referring to Glazer, William M.; Morgenstern, Hal; Doucette, John T. (1993). “Predicting the long-term risk of tardive dyskinesia in outpatients maintained on neuroleptic medications”. Journal of Clinical Psychiatry. 54 (4): 133–9. PMID 8098030 .
- ^ Jeste, Dilip V.; Caligiuri, Michael P.; Paulsen, Jane S.; et al. (1995). “Risk of Tardive Dyskinesia in Older Patients: A Prospective Longitudinal Study of 266 Outpatients”. Archives of General Psychiatry. 52 (9): 756–65. doi : 10.1001/archpsyc.1995.03950210050010 . PMID 7654127 .
- ^ Whitaker, Robert (2002). Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill. Perseus.[ page needed ]
- ^ Marshall, DL; Hazlet, TK; Gardner, JS; et al. (2002). “Neuroleptic drug exposure and incidence of tardive dyskinesia: A records-based case-control study”. Journal of managed care pharmacy. 8 (4): 259–65. PMID 14613418 .
- ^ Tarsy, Daniel; Lungu, Codrin; Baldessarini, Ross J. (2011). “Epidemiology of tardive dyskinesia before and during the era of modern antipsychotic drugs”. In Vinken, P. J.; Bruyn, G. W. Handbook of Clinical Neurology. Hyperkinetic Movement Disorders. 100. pp. 601–16. doi : 10.1016/B978-0-444-52014-2.00043-4 . ISBN 978-0-444-52014-2 . PMID 21496610 .
- ^ Jeste, Dilip V.; Caligiuri, Michael P. (1993). “Tardive Dyskinesia” . Schizophrenia Bulletin. 19 (2): 303–15. doi : 10.1093/schbul/19.2.303 . PMID 8100643 .
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