Management Of Tardive Dyskinesia Research Articles

A potential mechanism underlying the voluntary suppression of Tardive Dyskinesia

Many clinicians have observed that patients with tardive dyskinesia (TD) can voluntarily suppress the movements to some extent. The mechanism by which voluntary control is exerted most likely involves peripheral feedback. Quantitative analyses of isometric and isotonic jaw stability were conducted in patients with and without TD to test the general hypothesis that involuntary movements of TD may be brought under voluntary control via one of two receptor mechanisms; muscle length and/or muscle force. Results indicated that in the absence of length feedback patients with TD exhibited significantly greater instability while patients without TD performed within normal limits. This suggests that patients with TD utilized muscle length feedback to suppress motor instability but were unable to utilize muscle force feedback to suppress instability. Implications for the use of laboratory procedures in the measurement and clinical management of TD are discussed.

Overcoming institutional and community resistance to a tardive dyskinesia management program.

A growing body of research has examined psychiatry's previously hesitant response to the problem of tardive dyskinesia, but little has been said about resistance among institutions and communities to managing tardive dyskinesia. This paper describes how staff of a tardive dyskinesia management program overcame such resistance in both an inpatient and an outpatient setting and implemented tardive dyskinesia guidelines promulgated by an American Psychiatric Association task force in 1979. Through educational and liaison activities, the program staff overcame the fears of nurses and community sponsors of outpatients about reducing or withdrawing patients' neuroleptic medication. Implementation of the program required strong support from the hospital administration and an increase in communication between the various services and outpatient programs treating patients with tardive dyskinesia.

Management of Tardive Dyskinesia: Collected Articles From H&CP—prepared by the Hospital and Community Psychiatry Service, 1986, 40 pages, paperbound. Available from the H&CP Service, American Psychiatric Association, 1400 K Street, N.W., Washington, D.C. 20005, for $7.50, or for $5 each for five on more copies. (Orders of less than $35 must be prepaid.)

<b>Management of Tardive Dyskinesia: Collected Articles From <i>H&amp;CP</i>—prepared by the Hospital and Community Psychiatry Service, 1986, 40 pages, paperbound. Available from the H&amp;CP Service, American Psychiatric Association, 1400 K Street, N.W., Washington, D.C. 20005, for $7.50, or for $5 each for five on more copies. (Orders of less than $35 must be prepaid.)</b>

Tardive dyskinesia and informed consent

Tardive dyskinesia is a potentially irreversible neurologic syndrome secondary to long-term neuroleptic drug use. It is characterized by slow. rhythmical. automatic stereotyped movements particularly in the buccolingual masticatory area. extremities. and trunk muscles in patients who have received neuroleptic drugs for at least three months. Unlike other neurologic side effects to neuroleptic drugs, tardive dyskinesia is resistant to treatment with anticholinergic drugs. There is no generally effective treatment of tardive dyskinesia. I The prevalence of tardive dyskinesia varies widely in different studies but most likely is in the range of 10 to 20 percent of patients on maintenance neuroleptics. Of the total to to 20 percent of patients with tardive dyskinesia, less than to percent of them have severe abnormal movements with a fourth to a third of patients with the disorder showing moderately severe movements. While early studies suggested as many as 60 percent of cases of tardive dyskinesia were irreversible, more recent studies are more optimistic that frequent reversibility may be possible with early detection and discontinuation or reduction of neuroleptic medication. Confounding the detection and management of tardive dyskinesia is the fact that the very cause of the syndrome, neuroleptic drugs, also serves to mask it. Thus tardive dyskinesia is frequently not detected until the drugs are stopped or the dosage reduced. It is not clear what the relationship is between so-called withdrawal emergent dyskinesias and tardive dyskinesia that appears on a steady dose of neuroleptic. I However, it is clear that tardive dyskinesia is today a major public health issue in psychiatry.2 We are talking about a sometimes irreversible. sometimes severe, sometimes grotesque neurologic disorder induced by longterm exposure to what is currently the best and. to many minds, the only effective treatment for schizophrenia. It is no small wonder then that tardive dyskinesia has aroused a great deal of concern in the psychiatric community. Some have attempted to deny its existence, its irreversibility or its etiologic connection to neuroleptic

Management of tardive dyskinesia with thiopropazate.

The author describes the successful management of two severe cases of tardive dyskinesia with thiopropazate. He concludes that the drug does have a place in the management of tardive dyskinesia even though its mechanism of action and long-range effects are unknown. He cautions, however, that it should be used only in severe cases.

Prevention and management of tardive dyskinesia.

Because no adequate therapy is available, the prevention of tardive dyskinesia is of great importance. The disorder may be prevented by periodic evaluations of the neurologic status of patients on long-term drug treatment, followed by reducing the drug dosage or discontinuing administration. Withdrawing neuroleptics, particularly in patients with pseudoparkinsonism, may uncover latent dyskinesia. For patients already exhibiting this disorder, the use of small doses of neuroleptics may be safe, provided changes in neurological symptoms are monitored carefully.