Vigilant Screening for Tardive Dyskinesia Among Recommendations to Mitigate Symptom Severity

In Part 1 of this Q&A, Craig Chepke, MD, FAPA, adjunct associate professor of psychiatry for Atrium Health, adjunct assistant professor of psychiatry for The University of North Carolina School of Medicine, Chapel Hill, discusses patients living with Tardive Dyskinesia (TD) from his session entitled, “Tardive Dyskinesia Across the Complexity Spectrum—From Quality of Life Improvement to Novel Treatments," recently presented at the Psych Congress Elevate virtual meeting. 

Clinicians should be vigilant about screening patients for TD as earlier detection is key in improving or slowing illness severity, suggests Dr Chepke who is also the medical director of Excel Psychiatric Associates, Huntersville, North Carolina.

In the upcoming Part 2, Dr Chepke will expand on the key takeaways for clinicians for using the updated guideline recommendations and misconceptions surrounding TD.

Register for the 2022 Psych Congress Elevate taking place in Las Vegas, Nevada, June 3-5 by clicking here.

Question: How prevalent is TD in patients currently taking an antipsychotic medication?

Answer: The best evidence of the prevalence of TD comes from a 2017 meta-analysis by Carbon and colleagues. The estimated mean prevalence of TD with first-generation antipsychotic (FGA) use is 30%, compared with about 20% for those currently taking second-generation antipsychotics (SGAs). One caveat is that the studies used to calculate the latter number did not specify if patients had any prior treatment with FGAs, a key risk factor for developing TD. But even studies excluding previous FGA history, the estimated mean prevalence of TD was about 7% with pure SGA exposure. That might sound a lot better than 30%, but it’s still roughly 1 out of 14! If I were facing the possibility of a potentially irreversible movement disorder, I don’t like those odds. Furthermore, the number of people who are being prescribed antipsychotics has steadily and dramatically risen over the past few decades. So, even assuming a decreased incidence with SGAs, I’d posit that the rapid expansion of the pool of patients at risk for TD will soon nullify any advantage gained from SGAs, if it hasn’t already happened.

Q: What are the main ways TD impacts patient outcomes?

A: We must consider the impact of TD across the biopsychosocial spectrum. In my practice, I’ve seen physical complications in organ systems that we haven’t associated with TD historically. There can be difficulty breathing or speaking due to the involvement of muscles involved in respiration. Proper swallowing can be compromised, putting people at risk of possible aspiration. And gait impairment can increase the fall risk. Far from being merely a cosmetic illness, TD could be associated with excess medical morbidity and even potentially mortality. In the psychological domain, several studies have demonstrated an association of worse psychiatric symptoms and outcomes for people with TD. I’ve certainly treated many patients in whom I felt that TD was the chief contributing factor to their depression or anxiety.

TD can have a tremendous social burden and can be quite stigmatizing for those living with it. Appearances count for a lot in our society—humans can and will discriminate against any difference that can be seen or heard, and TD most commonly manifests in the most visibly prominent part of the body, the face. My patients have told me that they feared their TD would make them everything from “unemployable” to “unlovable.”

Q: What are the key strategies to mitigate symptom severity in patients with TD?

A: Of course, the best way to mitigate TD is to prevent it from developing in the first place! However, we can only use the tools we have available. Antipsychotics have such rich and diverse pharmacodynamic profiles that using them is often unavoidable, even in many patients without psychotic spectrum illnesses. Even so, I think we could do a better job as a field of using lower doses and shorter durations.

We should also be vigilant about pervasively screening our patients for TD. Earlier detection could limit the progression of its severity. Once we’ve diagnosed TD, there are some steps we can take to improve the severity of the illness. Generally, this does not have to include the old standby of reflexively discontinuing the antipsychotic. There isn’t good evidence this is beneficial in reversing TD, but it certainly puts the patient’s stability at substantial risk. I also wouldn’t advise switching to an antipsychotic with lower potency dopamine blockade. If a patient wasn’t already prescribed one of those agents, there’s generally a good reason for it.

However, if you want to remove something from the patient’s regimen, remember that TD is a state of dopamine hypersensitivity. Reducing medications that worsen TD by promoting dopamine transmission, either directly (like bupropion and stimulants) or indirectly (such as anticholinergics) is recommended.

Craig Chepke, M.D., FAPA, is an Adjunct Associate Professor of Psychiatry for Atrium Health, an Adjunct Assistant Professor of Psychiatry for The University of North Carolina School of Medicine, Chapel Hill, and the Medical Director of Excel Psychiatric Associates, Huntersville, North Carolina.