Tardive dyskinesia (TD) is a neurological syndrome associated with long-term use of antipsychotic (neuroleptic) drugs prescribed to treat psychiatric disorders, particularly schizophrenia, as well as some gastrointestinal or neurological conditions. It is characterized by involuntary, purposeless movements—often choreiform (rapid, jerky, nonrepetitive), athetoid (slow, sinuous, continual), or rhythmic (stereotyped). TD usually involves muscles of the mouth and face, although any muscle in the body can be affected. Many cases of tardive dyskinesia are mild and TD does not always progress in severity, though some people develop severe and disabling TD. The dyskinetic movements are permanent in about half of people who develop them, they and are diminished by action of the involved body part and may be increased by the action of unaffected body parts. Psychological stresses, including excitement and agitation, have been shown to increase dyskinetic movements, while relaxation and sedation reduce the severity.
Tardive dyskinesia usually appears late in the course of drug therapy. For many people with TD, symptoms can decrease or disappear with a decrease or discontinuation of the medication, although in some people symptoms may continue indefinitely. In addition, symptoms may not be observed until the antipsychotic medication is decreased or withdrawn, since tardive dyskinesia may be masked by the drug that has caused the disorder. Reports have associated TD with older neuroleptics, including haloperidol (Haldol), thiothixene (Navane), fluphenazine (Prolixin), chlorpromazine (Thorazine) ((Edelson)), thioridazine (Mellaril), and trifluoperazine (Stelazine).
Although supersensitivity of striatal dopamine (DA) receptors was previously thought to result in the development of TD, it now seems that several neurotransmitter systems may be affected. These include dopaminergic, noradrenergic, gamma-amino-butyric acid (GABA)ergic, cholinergic, and peptidergic pathways.
There is no standard treatment for tardive dyskinesia. Providers work with the individual and his or her family to create a plan unique to the individual that best addresses his or her needs. Routine monitoring is important to track changes and progress. In general, prevention is key—people at-risk should be assessed at frequent intervals for early signs of TD.
As of yet, there is no consistently beneficial pharmacologic therapy for TD, in spite of investigations of many drugs aimed at the dopaminergic, cholinergic, and GABAergic systems. New, atypical antipsychotics, including risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), sertindole (Serlect, Serdolect), ziprasidone (Geodon, Zeldox), and aripiprazole (Abilify, Abilitat), have been designed for use in place of older TD-causing antipsychotic drugs. It is yet to be determined clearly in clinical studies whether the long-term use of these atypical antipsychotics will lead to a lower incidence of tardive dyskinesia—risperidone has actually been associated with TD in some cases. Clozapine (Clozaril), an atypical antipsychotic agent rarely associated with tardive dyskinesia, was the first atypical antipsychotic to be used in place of TD-causing neuroleptics. Nonetheless, its use has been limited by a variety of other side effects, including agranulocytosis and the consequent need for a weekly monitoring of white blood cell counts, sedation, and seizures.
Medications with relatively few side effects that may suppress TD include calcium channel blockers (such as nifedipine), adrenergic antagonists, and vitamin E. Although vitamin E has not been proven definitively effective, it is commonly used and of minimal risk of toxicity. Treatment with the presynaptic dopamine depleters tetrabenazine (not available in the United States) and reserpine has met with fair success, but side effects have limited their use and the studies so far are of short duration. GABA agonists such as baclofen, valproic acid, or clonazepam may decrease hyperkinetic movements, but more studies are needed to support this conjecture.
Research is constantly underway in both the treatment and prevention of tardive dyskinesia, so physicians should conduct a thorough review of the most current studies and consider consulting a psychiatrist prior to prescribing treatment medications.
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The American Academy of Child and Adolescent Psychiatry
Phone: (202) 966-7300
American Academy of Neurology
Phone: (651) 695-2717
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Bazelon Center for Mental Health Law
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California Alliance for the Mentally Ill
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Tardive Dyskinesia/Tardive Dystonia National Association
Phone: (206) 522-3166
The Tarjan Center for Developmental Disabilities at UCLA
WE MOVE (Worldwide Education and Awareness for Movement Disorders)
Mt. Sinai Medical Center
Phone: (212) 241-8567
Phone: (800) 437-6682
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