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2024 Tardive Dyskinesia FAQ
Expert-Informed Strategies for Diagnosing and Managing Tardive Dyskinesia

Released: July 25, 2024

Expiration: July 24, 2025

Jeremy A. Schreiber
Jeremy A. Schreiber, MSN, APRN, PMHNP-BC
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Key Takeaways
  • Tardive dyskinesia (TD) is a hyperkinetic movement disorder that requires thorough assessment and visualization to diagnose.
  • Proactive consideration of risk factors in patients treated with dopamine receptor blocking agents can help to promptly identify TD and minimize its burden on patients.
  • Two FDA-approved VMAT2 inhibitors are effective, well tolerated, and should be considered for patients whose symptoms impact their quality of life.

In this commentary, Jeremy A. Schreiber, MSN, APRN, PMHNP-BC, provides answers to frequently asked questions from CCO’s 2024 Psychiatry Update for APPs series and discusses nuances and best practices in treating patients with tardive dyskinesia (TD) with considerations for special populations.

What are the key factors in differentiating TD from extrapyramidal symptoms (EPS) due to antipsychotic agents or other movement disorders like Parkinson’s disease, restless leg syndrome, or myoclonus?
Differentiating TD from other forms of EPS and other movement disorders often requires a thorough assessment and visualization of patients’ movements. The movements of TD are athetoid and/or choreiform (ie, writhing, snake-like, jerky, irregular). These movements are generally nonrhythmic, meaning there is no meter or cadence to their presentation. They can occur in just about any body area but are commonly observed in the face. These movements generally worsen if the prescribed antipsychotic is reduced or stopped. Further, TD is a hyperkinetic movement disorder.

Parkinson’s disease is not caused by antipsychotics, but drug-induced parkinsonism (DIP) can be caused by blocking postsynaptic dopamine receptors. Parkinson’s disease and DIP generally present with similar symptoms, such as tremor—but there is a rhythm and cadence to these movements, stooped posture, drooling, and/or masked facies (eg, diminished expression). Apart from tremor, the symptoms of these disorders are hypokinetic. 

Restless leg syndrome is often characterized by a strong desire to move one’s legs or an uncomfortable feeling that can potentially be reduced by moving. In general, patients report that these symptoms occur at night or when laying down.

Finally, myoclonus is a sudden jerking of a muscle. It is generally brief and sudden, such as a twitch or spasm, and cannot be controlled or reduced by the person experiencing it.

What are your tips for assessing TD-related symptoms via telehealth? 
The first tip would be to assess for TD and other movement disorders when prescribing medications that can cause them, as this is recommended by the American Psychiatric Association. Good practice would be first to probe for the presence of any type of movement. If possible, patients should be in a well-lit room and one should be able to view the whole patient, potentially asking a caregiver or family member to help by holding the camera and focusing in on various body areas of the patient if necessary. It is also a good idea to have a clear space for the patient to walk about, so they may be viewed walking from a distance. If you notice any type of movement, a more thorough assessment may be warranted.  

What strategies do you use for patient discussions on the potential severity of TD and the need for pharmacologic treatment? How do you have that conversation without scaring them?
Generally, when I am assessing the severity of TD, I probe the surrounding impact. In essence, how do the movements affect the patient’s life? The guidelines suggest that if TD affects the life of the patient, we should be treating them. I do not think that the TD conversation scares patients away; if anything, I think it is something that can offer improvement for their condition, although it sometimes requires several conversations until they become receptive to treatment. The FDA-approved VMAT2 inhibitors are efficacious treatments and generally well tolerated. 

How can TD treatment with a VMAT2 inhibitor be managed in patients who also need an anticholinergic agent (eg, benztropine to treat dystonia)?
I like this question because it implies that the anticholinergic is not being used to treat TD. If it were, I would first recommend tapering patients off of it. In the KINECT-3 trial of valbenazine, benztropine use was present in 34% of study participants. This being the case, I would feel comfortable using valbenazine in patients who were also treated with benztropine. In the clinical trials evaluating deutetrabenazine (ARM-TD and AIM-TD), patients were excluded if they were also on benztropine. Because there is not a body of evidence to support using deutetrabenazine in this patient population, I would avoid using this combination.  

Do you have any guidance on the preventive use of VMAT2 inhibitors for patients being treated with antipsychotics before TD-related symptoms can develop?
Currently there is no guidance on using VMAT2 inhibitors prophylactically to reduce the potential to develop TD. That being said, the risk factors that increase the likelihood of developing TD should be taken into consideration. Postmenopausal women, patients aged 55 years or older, and those with history of chronic substance use are at higher risk of developing TD. Longer duration and/or higher potency of dopamine receptor blocking treatment also increases the risk, as does treatment with anticholinergic agents. This is not a comprehensive list of risk factors, but it is a good starting point to identify patients for more careful monitoring.  

Can VMAT2 inhibitors be used in patients with Parkinson's disease?
Patients with Parkinson’s disease are especially sensitive to reductions in dopamine transmission. Deutetrabenazine and valbenazine do not have label contraindications for Parkinson’s disease but do carry warnings for the potential development of parkinsonism, therefore I would not recommend using these agents in patients with Parkinson’s disease. There may be instances in clinical practice where a VMAT2 inhibitor could be considered in patients who also have Parkinson’s disease, but I would entrust this use to an expert as addition of a VMAT2 inhibitor can potentially exacerbate Parkinson’s disease symptoms, potentiate falls, increase tremor, or worsen gait disturbances.

What is known about VMAT2 inhibitors’ impact on the natural progression of TD? Will symptoms return if treatment is discontinued?
There is some debate about the natural progression of TD in individuals who develop this condition, whether it be its potential to worsen or hold steady over time, and the impact of VMAT2 inhibitors is unknown. To ascertain this, we would need a study including an enormous number of participants for a duration that would likely not be economically feasible to measure. We do know that both valbenazine and deutetrabenazine are efficacious and generally well tolerated. In 2 clinical trials with valbenazine, patients’ Abnormal Involuntary Movement Scale (AIMS) scores, in aggregate, increased when they stopped the medicine. In clinical practice, I have seen patients on both valbenazine and deutetrabenazine experience an increase in movements when treatment is discontinued, as well as a reduction in AIMS scores when treatment is subsequently resumed.  

What factors should be considered when choosing between deutetrabenazine vs valbenazine?
Both valbenazine and deutetrabenazine are currently available as a single pill taken once a day, and valbenazine is also available as a sprinkle formulation that can be added to soft foods. Valbenazine’s full dosage range is considered therapeutic, whereas deutetrabenazine must be titrated to its therapeutic dosage. Both agents have dose restrictions in patients who are poor metabolizers of CYP2D6 or are on strong inhibitors of CYP2D6 (valbenazine, 40 mg max dosage; deutetrabenazine, 36 mg max dosage). In addition, valbenazine has a dose restriction for patients who are on strong CYP3A4 inhibitors (40 mg max dosage), and it is recommended that patients not be concomitantly taking strong CYP3A4 inducers or monoamine oxidase inhibitors. Further, deutetrabenazine is not recommended in patients with hepatic impairment, and valbenazine has a dose restriction (40 mg max dosage) in patients with moderate or severe hepatic impairment. Therefore, the determination should consider these factors as well as patient characteristics and preference.

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