What’s New in Tardive Dyskinesia, With Jonathan Meyer, MD

At the 2025 Southern California Psychiatry Conference at Huntington Beach, CA, from July 11 – 12, Jonathan Meyer, MD, presented on muscarinics and tardive dyskinesia (TD).

In an on-site interview with Psychiatry Times, a brand under MJH Life Sciences, Meyer, a voluntary clinical professor at the University of California, San Diego, discussed what’s new in tardive dyskinesia, when to switch medications, and how the only effective treatment for this condition is VMAT2 inhibitors.

In this Q&A, Meyer emphasized the importance of making sure you diagnose tardive dyskinesia correctly, not mixing up tardive dyskinesia with Parkinsonism. Medications for Parkinsonism worsen tardive dyskinesia symptoms, and vice versa. Only 2 FDA-approved medications for tardive dyskinesia sit on the market—tetrabenazine and valbenazine—both vesicular monoamine transporter 2 (VMAT2) inhibitors.

What's new in tardive dyskinesia?

Meyer: The big thing that's new is not the medications. We've had two FDA-approved treatments in 2017, but in the early days when they're just approved, I think the focus was more on detecting tardive dyskinesia. We've come to appreciate that it's not just the movements, it's the functional impact, the impact on the person's well-being, the impact on psychosocial functioning.

A big aspect of what I'll be covering today is really how to use some of these newer instruments that have been developed to help you figure out for your patients with TD, how it interferes with what they do on a day-to-day basis, not just physically, but psychologically and socially.

If you have a patient and you're giving the medication for TD, and you don't see that they're improving, what are some of the things that clinicians should be thinking about?

Meyer: Well, for one thing, you want to make sure that you have the right diagnosis. There are sometimes movements [that] can happen to people on psychotropic [medications], which may lead the clinician to think they have tardive dyskinesia.

A classic example is a form of Parkinsonism, in which the person has jaw tremors, because it's in this area, we often would assume it's tardive dyskinesia, and most of the time, you're right…if they've been exposed to a D2 blocker, but in this case, it's actually a form of Parkinsonism. The medicines [that] make Parkinsonism better tend to make TD worse. Conversely, for people with Parkinsonism, the medicines for TD tend to make those symptoms worse.

If you assume, though, that you have the correct diagnosis, the most important thing is making sure the person's taking the medication and that you've maximized the dose. If there is no response whatsoever on the maximal dose of one medication, there's really no harm in trying the other one. We only have 2 options right now, which are FDA-approved, but there are a subset of people with TD who don't get adequate improvement with either of the 2 FDA-licensed medications. Those are the types of people who you may refer to a neurologist for further evaluation and treatment.

Between the two, how should a clinician decide which one they're going to start trying? Is there a rhyme or reason to it?

Meyer: There really often isn't. One of them has a bit more of a titration schedule, which is tetrabenazine. Does that always cause a problem? Not necessarily. There are actually some people who prefer a lower initiation schedule.

Valbenazine is easier to initiate. 40 milligrams is the starting dose, and it's actually a very effective dose. I say to clinicians: you need to know how to use both, simply because insurance, more than anything, may dictate what you have access to. They are both effective.

We don't have any head-to-head data. There's inferential data from imaging studies that maybe you might get more VMAT2 occupancy, perhaps at the maximal dose of valbenazine versus the maximal dose of tetrabenazine. I can't promise there's always a clinical correlate for that, but it emphasizes a point of [knowing] how to use both. Maybe somebody will respond better, or perhaps a differential tolerability to one or the other.

Any closing thoughts that you want to share with clinicians?

Meyer: The only effective treatments for tardive dyskinesia are the VMAT2 inhibitors. In the old days, people used to throw medicines like benztropine against all movement disorders with the D2 blockade. We now know that they're not effective for TD, and in fact, they tend to make it worse.

The only thing I'll say about that is, if you have people on anticholinergics at some point in their treatment, if they have TD, you want to slowly taper them off to allow the VMAT2 inhibitor to give you your maximum benefit for their movements, most importantly, to improve their quality of life related to their tardive dyskinesia.