Tardive Dyskinesia 

  • Author: James Robert Brasic, MD, MPH; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: Jan 21, 2010
 

Background

Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications. Although they are associated with the use of neuroleptics, TDs apparently existed before the development of neuroleptics. People with schizophrenia and other neuropsychiatric disorders are especially vulnerable to developing TDs after exposure to conventional neuroleptics, anticholinergics, toxins, substances of abuse, and other agents. TDs are most common in patients with schizophrenia, schizoaffective disorder, or bipolar disorder who have been treated with antipsychotic medication for long periods, but TDs occasionally occur in other patients as well. For example, people with fetal alcohol syndrome, other developmental disabilities, and other brain disorders are vulnerable to the development of tardive dyskinesias, even after receiving a single dose of the causative agent.

TDs may be differentiated from acute movement disorders that commonly occur in the same patient groups. The acute movement disorders that occur as manifestations of effects of neuroleptics and other dopamine antagonists include akathisia, acute dystonia, and other hyperkinetic dyskinesias. Acute effects of dopamine antagonists also include Parkinsonian syndromes manifested by bradykinesia, rigidity, and pill rolling tremor. The acute movement disorders resulting from exposure to dopamine antagonists are commonly termed extrapyramidal syndromes (EPS).

The occurrence of acute movement disorders upon exposure to dopamine antagonists is increased in female patients and older patients. Use of potent dopamine antagonists, prolonged exposure to dopamine antagonists, and prior occurrence of acute movement disorders on exposure to dopamine antagonists are also associated with an increased risk for the occurrence of acute movement adverse effects. Withdrawal dyskinesias may also occur as treatment with dopamine antagonists is decreased or withdrawn. They are often refractory to all therapeutic modalities. In addition to the prototypic orofacial dyskinesia, tardive syndromes also include a spectrum of hyperkinesias occurring during or after prolonged treatment with dopamine antagonists.

Bishnoi and colleagues provided evidence of the involvement of the adenosinergic receptor system in the development of TD in rodents. Haloperidol induced vacuous chewing movements, orofacial movements, and facial stereotypies in rate. These changes were reversed after treatment with adenosine or caffeine. These findings provide evidence that adenosine, a major inhibitory neurotransmitter in the central nervous system, plays a role in TD. Additionally, these results suggest potential therapeutic agents for clinical trials.[1]

Bishnoi and colleagues have demonstrated a beneficial effect of progesterone on an animal model of tardive dyskinesia. They hypothesize that the favorable effect of progesterone is modulated by means of the GABAergic and neuroprotective actions of alloprogesterone, a metabolite of progesterone.[3]

TD has been associated with polymorphisms of both the dopamine receptor D2 (DRD2) gene[2] , TaqI A and TaqI B and associated haplotypes[4] , and of the dopamine receptor D3 (DRD3) gene[2, 5] , the dopamine transporter (DAT) gene, and the manganese superoxide dismutase (MnSOD) gene.

Dysfunction of the dopamine transporter has been hypothesized to play a role in the development of TD. However, Lafuente and colleagues did not find evidence of involvement of a polymorphism with a variable number of tandem repeats (VNTD) in the DAT gene (SLC6A3) in dyskinesias induced by antipsychotics.[6] Thus, further research is needed to investigate the role of the dopamine transporter in the development and maintenance of TD.

Galecki and colleagues have reported the association of a polymorphism of the manganese superoxide dismutase (MnSOD) gene and TD.[7]

Please find the following tools associated with this article: Abnormal Involuntary Movement Scale, Psychoactive Medication Quality Assurance Rating Survey, Psychoactive Medication Quality Assurance Rating Survey Screening Criteria, Hillside Akathisia Scale, Movement Disorders Checklist, Definitions of Indicator Functions Utilizing the Items of theMovement Disorders Checklist, Algorithms to Classify Movement Disorders, Timed Stereotypies Rating Scale, Audio Segment.

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Pathophysiology

For most of the past century, movement disorders (ie, abnormal adventitious movements) have been categorized as extrapyramidal syndromes (EPSs) due to lesions of the extrapyramidal system of the central nervous system. The pyramidal system, controlling voluntary movements, includes precise anatomic pathways from the cortex to muscle. Voluntary movements through the pyramidal systems are visible. By contrast, extrapyramidal motor activities result in automatic movement and static, postural movement activities that are not noticeable. The extrapyramidal system includes theorized connections within the basal ganglia, the striatopallidonigral system, and other structures of the central nervous system that contribute to the regulation of movement, including related brainstem nuclei and the cerebellum.

An example of a classic disorder of the pyramidal system is a stroke, resulting in paralysis of an extremity. Corticospinal lesions above the pyramidal decussation typically result in paralysis of volitional movements of the contralateral half of the body and a fixed posture with flexion of the upper extremity and extension of the lower extremity. Bilateral corticospinal lesions of the upper pons and midbrain typically cause extension of all 4 extremities and decerebrate rigidity with dorsiflexion of the cervical and thoracolumbar spine. Unilateral lesions of the upper pons and midbrain often result in extension of the ipsilateral arm and leg.

Extrapyramidal dysfunction

Classic disorders of the extrapyramidal system include a variety of involuntary movement disorders. Some of these movement disorders include dyskinesias such as akathisia, chorea, dystonia, myoclonus, stereotypy, tic, and tremor.

Table 1. Classic Characterization of the Pyramidal and Extrapyramidal Systems (Open Table in a new window)

CharacteristicPyramidalExtrapyramidal
AnatomyPrecisely demarcated pathways from cortex to muscleHypothesized pathways among basal ganglia and other structures of the central nervous system
Physiologic movementsVoluntaryInvoluntary
Pathologic movementsParalysis, paresis, hyperreflexia, and spasticityAkathisia, athetosis, ballism, chorea, dystonia, myoclonus, stereotypy, tic, and tremor

The pathophysiology of extrapyramidal disorders has been disputed because some extrapyramidal disorders may not involve lesions of the basal ganglia and, in addition, may not be involuntary. Because of the problems inherent in the concept of the extrapyramidal system, caution must be exercised in the classification of movement disorders as EPSs, and new approaches to the classification of movement disorders may be helpful.

Dyskinesia is a type of movement disorder that is subdivided into bradykinesias and hyperkinesias. Bradykinesias are characterized by abnormal slowness (eg, rigidity), difficulty initiating and terminating actions, and the masked facial expression of patients with Parkinson disease. Hyperkinesias are purposeless movements, including akathisia, chorea, dystonia, myoclonus, stereotypy, tic, and tremor.

The classification of movement disorders as bradykinesias and hyperkinesias is based on the observed phenomenology, etiology, and topography. Practitioners and researchers may be confounded by these classifications of movement disorders and may prefer instead to use clinical impressions. Methods of data analysis, including linear and logistic regression, linear discriminant function analysis, factor analysis, inverted factor analysis, tree approaches, dynamic clusters analysis, and principal component analysis, may facilitate the classification of these diseases.

Dopamine system

The pathophysiology of TD is not well understood. Central dopamine blockade is hypothesized to play a role in the pathogenesis of TD. Acute movement disorders are also hypothesized to result, in part, from the blockade of dopamine receptors by dopamine antagonists.

Several hypotheses have been proposed for the development of TD.

  • Striatal dopamine receptor supersensitivity may be responsible.
  • Chronic dopamine blockade may result in up-regulation of dopamine receptor responsiveness.
  • TD is hypothesized to result from compensatory supersensitivity of dopamine receptors following chronic blockade. Long-term blockade of dopamine D2 receptors in the basal ganglia by dopamine D2 antagonists (eg, neuroleptics) may produce TD.
  • When dopamine D2 -receptor blockade is reduced (even slightly), an exaggerated response of the postsynaptic dopamine D2 -receptor (even to low concentrations of dopamine) may result.
  • Striatal disinhibition of the thalamocortical pathway from imbalance of D1 and D2 receptors may be involved.
  • Neurodegeneration secondary to lipid peroxidation or excitotoxic mechanisms may be responsible.

Although the dopamine D2 receptor has traditionally been implicated in the pathogenesis of TD, mounting evidence indicates that, in some individuals, the dopamine D3, D4, and D5 receptors are involved.

Most likely, genetic traits produce a vulnerability to develop TD when a susceptible individual is exposed to particular agents. For example, the MscI polymorphism of the dopamine D3 receptor gene has been associated with the development of TD. Support for the hypothesis that TD may result from blockade of postsynaptic dopamine receptors in the basal ganglia and other parts of the brain exists in the form of the beneficial effects of increasing doses of neuroleptics for some patients with TD. Thus, dopamine antagonists may mask TD.

Increased dopamine transport (DAT) uptake after treatment with quetiapine has been reported with the amelioration of TD in a 67-year-old woman.[8]

Nicotine may play a role in the pathophysiology of TS. Cigarette smokers appear to have increased metabolism of dopamine D2 antagonists. Nicotinic agonists appear to relieve dyskinesias in some people with Tourette syndrome (see Tourette Syndrome), a condition characterized by the presence of motor and phonic tics (see Tourette Syndrome and Other Tic Disorders). The relationship between TD and the use of cigarettes and other nicotinic agonists remains to be clarified.

In 2005, Tan and colleagues reported an inverse correlation of plasma levels of brain-derived neurotrophic factor and dyskinetic movements in people with schizophrenia with TD.[9] Thus, brain-derived neurotrophic factor appears to have a protective effect in the nervous system against TD with people with schizophrenia.

Modestin and colleagues have observed that a fluctuating course of the illness characterizes people with tardive dyskinesia. They also report that length of illness is highly correlated with tardive dyskinesia.[10]

Bishoi and colleagues have noted that curcumin, an antioxidant, may prevent the development of dyskinesias induced in animals by dopamine receptor blocking drugs.[11]

Clinical presentation

Patients often have movement disorders that may actually represent a mixture or overlap of several dyskinesia disorders, as depicted in the diagram below.

Tardive dyskinesia. Venn diagram of the classificaTardive dyskinesia. Venn diagram of the classification of movement disorders.

Individuals treated with neuroleptics may demonstrate both acute and chronic effects, manifested by acute dyskinesias and TD. Individuals may simultaneously manifest akathisia and tics after long-term treatment with neuroleptics.

The diagnosis of acute and chronic dyskinesias may be difficult without a past history when seeing a patient for the first time. Precise documentation of a patient's complete movement history and medication history may facilitate accurate delineation of movement disorders. Therefore, a full neurologic and pharmacologic history may provide the basis to distinguish idiopathic Tourette disorder from acute medication-induced tardive tics.

Patients and families often cannot provide accurate histories; thus, firm diagnoses may be impossible. Because acute and tardive medication effects may occur simultaneously, the distinction may be challenging in a clinical setting. Observing patients carefully on a regular basis with precise documentation at each visit, through structured rating instruments, of the phenomenology and topography of movements and the pharmacologic treatments helps to provide a basis for accurate future diagnosis of acute and TDs.

Genetic influences

A genetic basis for TD has not been identified. In particular, a functional polymorphism of the gene coding for human glutathione S-transferase P1 (GSTP1) does not appear to be associated with TD.[12] Additionally, CYP3A4 and CYP2D6 gene polymorphisms are apparently unassociated with TD.[13] TD has been associated with polymorphisms of the dopamine D3 receptor Ser9Gly[14] and of the serotonin 2A[2] and 2C receptor genes[14, 2] .

Reports of associations between TD and polymorphisms of NADPH quinine oxidoreductase 1 (NQO1) and superoxide dismutase 2 (SOD2, MnSOD) genes have not consistently been confirmed by subsequent studies.[15]

General diagnosis

TD is common in individuals with psychotic disorders (eg, schizophrenias, schizoaffective disorders, bipolar disorders) who are treated with antipsychotic medications, especially dopamine antagonists, for many years.

Generally, TD is diagnosed if one of the following circumstances is present. Criteria for neuroleptic-induced tardive dyskinesia are listed in the image below.

Diagnostic criteria for neuroleptic-induced tardivDiagnostic criteria for neuroleptic-induced tardive dyskinesia.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 2 movements of at least mild intensity while taking a neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 1 movement of at least moderate intensity while taking a neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 2 movements of at least mild intensity within 4 weeks of the discontinuation of the neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 1 movement of at least moderate intensity within 4 weeks of the discontinuation of the neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 2 movements of at least mild intensity within 8 weeks of the discontinuation of a depot neuroleptic.
  • A person who has taken neuroleptics for at least 3 months (1 mo if older than 60 y) develops at least 1 movement of at least moderate intensity within 8 weeks of the discontinuation of a depot neuroleptic.
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Epidemiology

Frequency

United States

In 1997, Goetz estimated that tardive dyskinesia (TD) occurs in approximately 15-30% of persons who receive long-term treatment with neuroleptics.[16] TD is more likely to occur in individuals who have manifested acute adverse effects of exposure to dopamine antagonists. Frequency of the various subtypes varies markedly. For example, orofacial, buccolingual, and masticatory dyskinesias are common, but only 1-2% of people treated with dopamine antagonists develop tardive dystonia.

Orofacial TDs differ from peripheral TDs in the occurrence of comorbid acute movement disorders. Acute tremor, acute akathisia, and acute Parkinsonism are more common in people with peripheral TD. Distinguishing acute and TDs in an individual patient can represent a serious diagnostic challenge.

The prevalence of TD is higher in cigarette smokers.[17]

International

The international frequency is apparently similar to that of the United States.

Race

Tardive dyskinesia (TD) occurs in persons of every race.[18]

  • Studies in different populations have identified overall prevalences of 1-65%.
  • Africans and African Americans appear to be especially vulnerable to TD after exposure to low doses of neuroleptics for short durations.
  • However, drawing any conclusions on the basis of these results is difficult because different investigators conducted the studies in different settings. A number of other variables, such as therapeutic approaches, methodologic inconsistencies, diet, weather, and varied assessments, may also contribute to the differences in various racial groups.

Sex

Elderly female patients appear to be particularly susceptible.[18] Young men are prone to develop tardive blepharospasm and tardive dystonia.

Age

TD occurs in all ages.

  • In 2001, Connor et al found that 5.9% of 95 young people aged 7-21 years receiving dopamine antagonist treatment for 3 months had TD.[19]
  • Advanced age is a major risk factor for TD.[18] The prevalence of TD is 29% in elderly patients receiving dopamine antagonist treatment for 3 months and 26-67% in patients treated long term.
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Contributor Information and Disclosures
Author

James Robert Brasic, MD, MPH  Assistant Professor, Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine

James Robert Brasic, MD, MPH is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, and Movement Disorders Society

Disclosure: Taylor and Francis Royalty Independent contractor; Wolters Kluver/Lippincott Williams & Wilkins Royalty Independent contractor; National Alliance for Research on Schizophrenia and Depression Grant/research funds Other; National Institutes of Health Grant/research funds Other

Coauthor(s)

Brian Bronson, MD  Staff Physician, Department of Psychiatry, New York University Medical Center

Disclosure: Nothing to disclose.

Tristen T Chun  Division of Nuclear Medicine, Russell H Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel H Jacobs  MD, FAAN, Associate Professor of Neurology, University of Florida College of Medicine; Director for Stroke Services, Orlando Regional Medical Center

Daniel H Jacobs is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, and Society for Neuroscience

Disclosure: Teva Pharmaceutical Grant/research funds Consulting; Biogen Idex Grant/research funds Independent contractor; Serono EMD Royalty Speaking and teaching; Pfizer Royalty Speaking and teaching; Berlex Royalty Speaking and teaching

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Nestor Galvez-Jimenez, MD, MSc, MHA  Chairman, Department of Neurology, Program Director, Movement Disorders, Department of Neurology, Division of Medicine, Cleveland Clinic Florida

Nestor Galvez-Jimenez, MD, MSc, MHA is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society

Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Additional Contributors

This research is supported by the Essel Foundation, the National Alliance for Research on Schizophrenia and Depression (NARSAD), the Tourette Syndrome Association, Inc, the National Institutes of Health, and the Department of Psychiatry of Bellevue Hospital Center and the New York University School of Medicine, New York, New York. The cooperation of the Health and Hospitals Corporation of the City of New York is gratefully acknowledged.

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Diagnostic criteria for neuroleptic-induced tardive dyskinesia.
Tardive dyskinesia. Venn diagram of the classification of movement disorders.
Table 1. Classic Characterization of the Pyramidal and Extrapyramidal Systems
CharacteristicPyramidalExtrapyramidal
AnatomyPrecisely demarcated pathways from cortex to muscleHypothesized pathways among basal ganglia and other structures of the central nervous system
Physiologic movementsVoluntaryInvoluntary
Pathologic movementsParalysis, paresis, hyperreflexia, and spasticityAkathisia, athetosis, ballism, chorea, dystonia, myoclonus, stereotypy, tic, and tremor
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