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Mitigating risks in antipsychotic prescribing

April 1, 2011
by William M. Glazer, MD
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As tardive dyskinesia research continues, wise prescribers are taking careful progress notes

In 1980, while working in a community mental health center at Yale, I initiated what became the largest Tardive Dyskinesia (TD) Clinic in the United States 1. We treated and studied thousands of patients and we trained dozens of behavioral health professionals in the recognition and management of this iatrogenic movement disorder.

By 1992, after clozapine had appeared and risperidone was becoming available, I thought that our mission had come to an end-that the problem of TD had been solved with “second generation” antipsychotic (SGA) medications. I reasoned that if the newer antipsychotics indeed were less likely to cause acute, parkinsonian or extrapyramidal side effects, then TD would be virtually eradicated.

In fact, since I left Yale and closed the doors of the TD Clinic in 1994, the SGAs have almost replaced the older antipsychotics. Clinicians reported that were seeing substantially fewer acute and long-term movement disorders than they did when they prescribed the older antipsychotics. And a number of studies, mostly sponsored by pharmaceutical companies, agreed2. But most of these analyses were retrospective in nature, and the relatively high doses of Haldol used for comparisons raised questions about their validity.

Meanwhile, our relief about the reduced risk of TD was overshadowed by a new observation-the SGAs were associated with weight gain and elevations in blood sugar and cholesterol. By the late 1990s, so much attention was placed on these newer concerns that the concern about TD seemed to fade into the background. The warnings for TD applied to the SGAs just as they had to the older antipsychotics, but the average clinician simply assumed that the risk of TD had been mitigated.

Then came the Yale study

ABOUT the author william m. glazer, md, is president of glazer medical solutions ( of key west, fla., and menemsha, mass. he is a clinician, researcher, lecturer, and consultant, and has been a member of faculty of the departments of psychiatry at the yale and harvard schools of medicine.
William M. Glazer, MD, is President of Glazer Medical Solutions of Key West, Fla., and Menemsha, Mass. He is a clinician, researcher, lecturer, and consultant, and has been a member of faculty of the departments of psychiatry at the Yale and Harvard schools of medicine.

Recently, my colleague at Yale, Dr Scott Woods and I published a study3 that raises questions about the assumption that the risk of TD has been reduced with the SGAs. Our study measured prospectively the incidence of TD among individuals served at a mental health center at Yale who were treated mostly with SGAs. To our surprise, we did not find a clear-cut reduction in the risk of TD in this population. While some of the SGAs seemed less likely to cause TD compared to others, the SGA-treated group as a whole developed TD at a rate just slightly less than the group treated with the older antipsychotics that we measured years ago.

Without going into all the methodological issues, suffice it to say that our study was not definitive. We were concerned that many of these patients had been exposed to the older medications prior to our study, so we could not cleanly separate the role of the SGAs in the TD risk that we measured. Thus, we need an incidence study that includes patients who have received only SGAs to really answer the question.

But the results of our study serve as a reminder to clinicians that TD is alive and well today.

How should we be thinking about TD in 2011?

Today, the best management strategy for TD is prevention. Clinicians must try to limit patients' exposure to any antipsychotic medication. This is more challenging in 2011 than it was before 1990 because there are now far more approved indications for antipsychotic medications, including bipolar disorder and depression.

If the patient needs an SGA, one way to limit exposure is to try to keep the dose as low as possible and then, if TD appears, taper and stop it if possible. But in many patients with severe symptoms, withdrawal of the antipsychotic may not be possible. To make matters more complicated, long-term dosing of the SGAs has hardly been studied4. Switching to clozapine or quetiapine is one option to consider in minimizing TD (again, there is no real evidence base to support this recommendation). There are no consistently effective drugs to treat TD, but I recommend Vitamin E, benzodiazepines, amantadine and beta-blockers.

Because TD is an iatrogenic, often-irreversible movement disorder, attention to risk management is tantamount.

Mitigating TD's legal risks: examination, risk/benefit ratio, and informed consent

As an expert witness in TD malpractice cases, I can say that the clinical and legal risks associated with antipsychotic prescribing are still very real. To mitigate these potentially expensive risks, it is important to address three themes in the progress notes for a patient who is receiving antipsychotic medications: examination, risk-benefit ratio, and informed consent.