Differential Diagnosis of Tardive Dyskinesia and Drug-Induced Parkinsonism

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Hi, I'm Dr Craig Chepke. I'm the medical director of Excel Psychiatric Associates in Huntersville, North Carolina, an adjunct associate professor of psychiatry for atrium health, and a steering committee member and a scientific director for Psych Congress.

When assessing for TD, it's critical to make sure that we are doing a differential diagnosis to make sure that we are actually diagnosing and treating tardive dyskinesia.

There has been an increase in the awareness and the ability and desire for clinicians to assess for TD in the past several years, and that delights me, but we don't want to jump to thinking that everything that moves is tardive dyskinesia, because that would be the pendulum swinging too far in the other direction. For too many decades, all we talked about was extra pyramidal symptoms (EPS) which is just a garbage basket diagnosis of pretty much any abnormal and voluntary movement. That's one thing that led down the pathway of us using anticholinergics like benztropine for everything that is an antipsychotic-related movement disorder.

The primary differential that most clinicians have to grapple with is tardive dyskinesia versus drug-induced Parkinsonism. Akathisia and dystonia, I think, most clinicians are able to tease out. Akathisia has that inner sense of restlessness, they can't stop moving, and they feel uncomfortable because of it. Dystonia is a sustained muscle contraction rather than intermittent movements in most cases.

So, it's TD versus Parkinsonism.

The way to differentiate one is the time frame. If you notice the symptoms come on right after an antipsychotic is started or increased in dosage or if you switch from a lower potency to a higher potency, that's one clue that it could be drug-induced Parkinsonism because that's an acute motor adverse reaction. Whereas tardive dyskinesia—tardive means just like the word “tardy,” if your kids are late for school, they're tardy.—tardive dyskinesia has late onset, months to years after starting the antipsychotic or other dopamine blocking medication.

In terms of the phenomenology of the movements themselves, you can differentiate. Movements of TD are a chorea form or athatoid, so dance -like, worm -like, snake -like, they're usually slower, although they can be fast in some cases, but usually slower, and they're not rhythmic.

In drug-induced Parkinsonism, generally, Parkinsonism is a slowness of movement—bradykinesia, akinesia,—but they can have some kind of islands, I call them, of hyperkinetic movements. Movements usually in the hands (the pill-rolling tremor), in the lips (a rabbit tremor where the lower lip kind of vibrates sometimes), you can get a titubation which is kind of like a bobblehead that the head bobbles about. But, what you have to remember is: number one, it's a tremor, and any tremor is perfectly rhythmic whereas the movements of TD are not rhythmic. They may have a pattern, but you can't exactly predict what they're going to be based on what they did in the past 5, 10, or 30 seconds like you can with a tremor because a tremor repeats itself more or less infinitely.

Then also, look at the whole person.

We'd always need to think about the whole person in many aspects but one is in this differential as well because as I mentioned Parkinsonism is usually slowness of movements and reduced movements. So even if we do see a hyperkinetic movement in their hands and in their lips, what's going on in between the two? Does the rest of their body not move very much when they walk? Do they have no arm swing and take small slow steps? Does the rest of their face, other than their lips, have no movement whatsoever and it looks like they've been over-botoxed?  They don't have any wrinkles on their face? They don't blink. Things of that nature.

Don't get into a staring contest with someone with Parkinsonism, you'll never win because they can't blink. Whereas with TD, they have either normal movements or excess movements throughout the body as opposed to the juxtaposition of some parts of having too many movements and some parts having too few.

So, those would be 3  of the ways that I would make that differential, and it's critical because making the right diagnosis is going to dictate your treatment, and treatment for one, could worsen the other. The VMAT-2 inhibitors, the approved and recommended treatments for TD, can cause drug-induced Parkinsonism in some people. And anticholinergics like benztropine, which can be used and are approved for drug-induced Parkinsonism, have the potential to worsen TD.

But also remember one more time, benztropine and other anticholinergics are not the only treatments for drug-induced Parkinsonism. Amantadine is also approved and very useful and does not have many of the adverse reactions that benztropine has. It does have adverse reactions we have to watch for, but it's my medication of choice if I'm treating drug-induced Parkinsonism.