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Tardive dyskinesia

Tardive dyskinesia is a serious neurological disorder caused by the long-term and/or high-dose use of dopamine antagonists, usually antipsychotics and among them especially the typical antipsychotics. These neuroleptic drugs are generally prescribed for serious psychiatric disorders. The older typical antipsychotics, which appear to cause tardive dyskinesia somewhat more often than the newer atypical antipsychotics, are being prescribed less frequently. There are some new uses, however, such as year-long implants that are being developed using the older typicals, e.g. more...

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Medicines

, Haldol®, one of the worst offenders when it comes to tardive dyskinesia. Other dopamine antagonists that can cause tardive dyskinesia are drugs for gastrointestinal disorders (for example metoclopramide) and neurological disorders. Some drugs that are not intended to affect dopamine, such as SSRI antidepressants, may also cause tardive dyskinesia. The new generation of atypical antipsychotics appears to cause tardive dyskinesia somewhat less frequently (though they may cause serious metabolic disorders, e.g., diabetes, frequently enough to make them equally dangerous).

The term tardive dyskinesia was introduced in 1964. Dyskinesia means "abnormal movement" and tardive means "late", signifying that the dyskinesia only occurs after some time has elapsed following initial administration of the neuroleptic drug.

Features

Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements. Features of the disorder may include grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid movements of the arms, legs, and trunk may also occur. Impaired movements of the fingers may appear as though the patient is playing an invisible guitar or piano. Many of the symptoms of tardive dyskinesia appear similar to Parkinson's disease.

Cause

The cause of tardive dyskinesia appears to be related to damage — due to the use of antipsychotic medications — to the system that uses and processes the neurotransmitter dopamine. It is thought that postsynaptic dopaminergic receptors become supersensitive to stimulation during neuroleptic treatment and that this supersensitivity causes the symptoms of tardive dyskinesia. The available research seems to suggest that the concurrent prophylactical 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.

Treatment

Primary prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. If tardive dyskinesia is diagnosed, the causative drug should be reduced or discontinued if possible. Tardive dyskinesia may persist after withdrawal of the 'offending neuroleptic' for months, years, or even permanently. There is no known cure for tardive dyskinesia, but preliminary research suggests that the atypical neuroleptic Clozaril (Clozapine®) may improve the state of the patient. Improvements are also seen in some cases, if the high potency benzodiazepines - lorazepam (Ativan®), diazepam (Valium®), or clonazepam (Klonopin®)—are used. The findings about the effects of natural substances, such as vitamin E (Alpha-Tocopherol) or melatonin, are inconclusive. Treatment with adrenergic blocking agents and dopamine agonists like bromocriptin also remains somewhat controversial. There have been some reports of promising effects from the drug tetrabenazine (a different kind of neuroleptic). On the contrary, most antiparkinsonian drugs worsen the state of the patient.

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Does Risperidone Induce Persistent Tardive Dyskinesia?
From American Family Physician, 1/15/01 by Karl E. Miller

One of the more common side effects from conventional neuroleptics is tardive dyskinesia. This side effect can be a significant problem because it tends to persist and is sometimes irreversible. Two risk factors for this side effect include older age and the cumulative neuroleptic amount. The one-year incidence of cumulative tardive dyskinesia reported in the literature is approximately 25 percent. The atypical antipsychotic agent risperidone has a much lower incidence of this side effect. However, few studies have looked at long-term therapy with this agent. Jeste and associates studied the incidence of tardive dyskinesia in elderly patients with dementia who are being treated with risperidone.

Patients with Alzheimer's disease, vascular dementia or mixed dementia who had indications for neuroleptic therapy were enrolled in a one-year, open-label study. They were evaluated at baseline and every two months. Dosages of risperidone were 0.5 to 2.0 mg per day, based on patients' response. Persistent emergent tardive dyskinesia was defined by the scores on the dyskinesia subscale of the Extrapyramidal Symptom Rating Scale. Among the 330 patients enrolled in the study, the mean age was 82.5 years. The mean dosage of risperidone was 0.96 mg per day, and the median length of use was 230 days. The one-year accumulative incidence of persistent tardive dyskinesia in patients without dyskinesias at baseline was 2.6 percent. Patients with dyskinesia symptoms at baseline experienced a significant reduction in the severity of their symptoms during the study period. Patients who received 0.75 to 1.5 mg per day of risperidone showed the best improvement in psychopathologic symptoms over the study period.

The authors conclude that the incidence of persistent tardive dyskinesia with risperidone treatment for psychopathology in elderly patients with dementia seemed to be much lower than the incidence in those treated with conventional neuroleptics. The average optimal dosage of risperidone in elderly patients with dementia is 0.75 to 1.5 mg per day.

2000;157:1150-5.

COPYRIGHT 2001 American Academy of Family Physicians
COPYRIGHT 2001 Gale Group

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