NORD gratefully acknowledges 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.
Tardive dyskinesia is characterized by involuntary and abnormal movements of the jaw, lips and tongue. Typical symptoms include facial grimacing, sticking out the tongue, sucking or fish-like movements of the mouth. In some cases, 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 is caused by long-term use of a class of drugs known as neuroleptics. Neuroleptic drugs are often prescribed for management of certain mental, neurological, or gastrointestinal disorders. Metoclopramide and prochlorperazine are drugs used for chronic gastrointestinal conditions that may cause tardive dyskinesia. Neuroleptic drugs block dopamine receptors in the brain. Dopamine is a neurotransmitter which is a chemical that helps brain cells to communicate. Although most cases occur after a person has taken these drugs for several years, some cases may occur with shorter use of neuroleptic drugs.
Tardive dyskinesia affects individuals who have been taking neuroleptic drugs for a long period of time. A high percentage of schizophrenic people who have spent long periods of time taking these drugs have a high risk of developing TD. However, neuroleptic drugs are also prescribed for depression, some digestive disorders, and other neurologic illnesses.
Treatment of tardive dyskinesia initially consists of discontinuing the neuroleptic drug as soon as involuntary facial, neck, trunk, or extremity movements are identified in people taking neuroleptic drugs if this is felt to be safe psychiatrically. Use of an “atypical” neuroleptic drug is often used in place of traditional neuroleptics if felt to be psychiatrically appropriate. However, the “atypical” neuroleptic drugs are also capable of causing or perpetuating tardive dyskinesia. In some cases, physicians may be forced to reinstitute a neuroleptic drug if the tardive dyskinesia symptoms do not disappear and become very severe after medication is discontinued.
Studies are ongoing to determine possible new drug therapies for the treatment of tardive dyskinesia. Choline, lithium, bromocriptine, baclofen, methyldopa, valproate, clonidine, propranolol, amantadine, clonazepam, and nifedipine have occasionally been helpful but in most cases do not improve dyskinesia. Tetrabenazine is often useful for symptomatic treatment of tardive dyskinesia and is currently available for use in the US. However, it carries the risk of causing or aggravating depression. Other experimental drugs are being tested to reduce or eliminate the symptoms of tardive dyskinesia. For more information about these studies, please contact the agencies listed in the Resources section of this report.
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:
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Brasic, JR. Tardive Dyskinesia.Medscape. Updated: Jul 17, 2014. http://emedicine.medscape.com/article/1151826-overview Accessed May 14, 2015.
NINDS Tardive Dyskinesia Information Page. Last updated April 18, 2014. http://www.ninds.nih.gov/disorders/tardive/tardive.htm Accessed May 14, 2015.
Online Mendelian Inheritance in Man (OMIM). Victor A. McKusick, Editor; Johns Hopkins University, Last update 03/31/2009. Entry Number 272620. Available at: http://omim.org/entry/272620 Accessed May 14, 2015.
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