Jonathan Meyer, MD, is a clinical professor of Psychiatry at UC San Diego and nationally recognized psychopharmacology educator.

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 

, 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.

 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?

 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?

 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?

 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.

Articles

Jonathan Meyer, MD, presented insights on tardive dyskinesia (TD) at the 2025 Southern California Psychiatry Conference. He emphasized the importance of accurate diagnosis, distinguishing TD from Parkinsonism, as treatments for one can exacerbate the other. The only FDA-approved treatments for TD are VMAT2 inhibitors, tetrabenazine and valbenazine. Meyer highlighted the need to assess the functional impact of TD on patients' lives and suggested trying both medications if one proves ineffective. He advised tapering off anticholinergics to maximize the benefits of VMAT2 inhibitors.

Discover the latest insights on tardive dyskinesia treatment, diagnosis, and the role of VMAT2 inhibitors in enhancing patient well-being.

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

Gus Alva, MD, previews the SoCal Psych agenda with faculty member Jonathan Meyer, MD.

 The Gus Alva Perspective: SoCal Psych Preview—Updates in Tardive Dyskinesia, with Jonathan Meyer, MD

2025 Southern California Psychiatry Conference

, host Gus Alva, MD, welcomes back Jonathan Meyer, MD, clinical professor of Psychiatry at UC San Diego and nationally recognized psychopharmacology educator, to discuss his upcoming session on tardive dyskinesia (TD)—a topic that remains under-recognized and under-treated in clinical practice.

With a pair of VMAT2 inhibitors now approved by the US Food and Drug Administration, the conversation around TD is shifting from basic identification to proactive management. Meyer emphasizes that the true burden of TD often lies not in the motor symptoms themselves, but in the psychosocial toll it takes. “It’s not just a movement disorder,” he says. “It’s a disorder of people.” Whether it's embarrassment at work, difficulty with social connection, or emotional distress, even mild TD can become deeply disruptive.

The session will also cover the complex care scenarios clinicians frequently face: coexisting drug-induced Parkinsonism, the inappropriate use of anticholinergics, and the challenge of treating TD without destabilizing psychiatric progress. Anticholinergics, Meyer notes, can make TD worse but often remain in treatment regimens.

Clinicians will also get an update on how to measure functional impairment beyond AIMS scores, and why having the right conversation with patients is key to avoiding dangerous decisions like stopping antipsychotic medications altogether.

Don’t miss Meyer’s deep dive into the clinical, emotional, and therapeutic layers of tardive dyskinesia—a conversation designed to equip every attendee with tools they can use immediately.

Podcasts

Jonathan Meyer, MD, previews his session on updates in tardive dyskinesia at the upcoming 2025 Southern California Psychiatry Conference.