Making a Diagnosis of Tardive Dyskinesia
Listen in as Dr Richard Trosch and Dr Cynthia Comella, both movement disorder specialists, discuss their approaches to recognizing tardive dyskinesia in their patients.
This podcast, “Making a Diagnosis of Tardive Dyskinesia,” is a promotional educational program sponsored and co-developed by Neurocrine Biosciences and is not certified for continuing medical education. The speakers are presenting on behalf of and are paid consultants for Neurocrine Biosciences. The information presented is consistent with FDA guidelines.
Dr Trosch: Hi, I’m Richard Trosch, a neurologist and movement disorder specialist practicing in Michigan. I’m an Associate Professor of Neurology at Oakland University and have an interest in tardive dyskinesia.
Dr Comella: And I’m Cynthia Comella, a Professor Emeritus at Rush University Medical Center in Chicago. I specialize in movement disorders, with a particular interest in tardive dyskinesia.
Dr Trosch: Today we’re going to talk about the key characteristics that help identify tardive dyskinesia and differentiate it from other movement disorders such as drug-induced parkinsonism.
Dr Trosch: Cindy, what steps do you take to recognize tardive dyskinesia early in your patients?
Dr Comella: Well, first I establish whether they’ve been on any of the agents that can cause tardive dyskinesia, such as the first- or second-generation antipsychotics and some antiemetics that block dopamine receptors.1,2 Because you really can’t have tardive dyskinesia without that exposure.3
Once that’s established, I go further into history and look closely at the patient. With tardive dyskinesia, you’ll see it often around the mouth area,4 so that’s where I focus first.
I ask the caregiver and the patient if they’ve noticed any difficulties with talking or swallowing.5 And then I do a neurologic exam to look for any abnormal involuntary movements elsewhere in the body, such as the neck, trunk, and upper and lower extremities.5
Dr Comella: How do you recognize tardive dyskinesia early, Rich?
Dr Trosch: Well, my tardive dyskinesia exam starts as soon as the patient is called to the exam room, because I’m watching the patient as they are walking down the hall and getting into the room, and as I’m taking the history.
I’m watching their eyes and how frequently they’re blinking.5,6 I’m watching their facial expression, and I’m watching their mouth movements as I’m talking to them. It’s not normal for patients to have bridling, tongue protrusion, chewing movements, or lip smacking.5,6 It’s not normal for them to be akathitic, moving in their chair, adjusting their posture, or getting up and pacing.5
So by the time I’m ready to conduct the physical exam, I’ve got a pretty good idea if they have tardive dyskinesia.
And if I do suspect tardive dyskinesia, I might ask them questions like5-7: Are you restless? Do you have trouble at night with labored breathing, or do you have trouble falling asleep because you’re restless? Can you sit through a meal? Are you biting the insides of your mouth, or biting your tongue and cheeks? Or, do you have dry mouth, or dry lips because you’re licking your lips all the time?
Dr Comella: And what about the role of the patient or caregiver in identifying tardive dyskinesia, in between visits?
Dr Trosch: Good question. I can’t tell you how many patients I’ve seen come in already on a neuroleptic, and I ask them: “Do you know what tardive dyskinesia is? Do you know that you’re on this neuroleptic medication that can cause these movements?” And some don’t know anything about it. And that always shocks me.
Because waiting the 3 or 6 months between our visits to identify tardive dyskinesia can be too long. We have to educate patients and caregivers about the risk of tardive dyskinesia and what it looks like, so they’re assessing it daily in between visits.3
Dr Comella: Agreed. I explain to patients and caregivers the movements they should be looking out for, and then I’d advise that if these movements become more pronounced, they should reach out for an appointment sooner than the one we’ve scheduled.
Dr Trosch: You have to look at the patient history. You can’t just look for movements.
Dr Comella: Right. The Abnormal Involuntary Movement Scale, commonly known as the AIMS, is often used to document the location and severity of movements.8 To identify tardive dyskinesia specifically, you really have to consider the type of movements.9
Dr Trosch: Let’s talk a bit about distinguishing tardive dyskinesia from drug-induced parkinsonism.
Dr Comella: So, tardive dyskinesia is typically hyperkinetic movement. Often, it’s got a stereotypy or repeating nonpurposeful component to it, such as lip smacking. Or it can be choreiform, where the movement is unpredictable. It can also be dystonic, where there’s patterned abnormal movement.5,9
With drug-induced parkinsonism, you get a very rhythmic tremor, typically associated with slowness and decrementing movements, which is bradykinesia. And a lot of times, you’ll see that the stride length is shortened. It’ll be a more shuffling gait.5,9
Dr Trosch: Right. So simply, tardive dyskinesia is a hyperkinetic movement disorder, and drug-induced parkinsonism is a hypokinetic movement disorder. So they’re actually opposites. With tardive dyskinesia, there’s way too much movement, and with drug-induced parkinsonism there’s a paucity of movement.5
Dr Comella: I think the potential confusion is around tremor. So tremor is associated with drug-induced parkinsonism and is sometimes called hyperkinetic, whether or not it should be. But the difference is that tremor in drug-induced parkinsonism is very rhythmic, versus irregular movements seen in tardive dyskinesia.9
Dr Comella: What about the onset of movements as a differentiator between the 2 disorders?
Dr Trosch: Well, drug-induced parkinsonism usually begins within weeks or months of neuroleptic exposure, and it’s dose related.9,10 And typically, reducing the dosage can diminish the severity over time.9
In contrast, most people with tardive dyskinesia get it after prolonged exposure to a neuroleptic,9,10 although I have personally seen it occur after a brief exposure. And for most people, tardive dyskinesia is more persistent and has a low remission rate.9,11 Reducing the neuroleptic dose once the patient has had tardive dyskinesia really does not help.9
Dr Comella: In fact, sometimes you see movements emerge as you reduce the dose of a dopamine receptor antagonist, which is very suggestive of tardive dyskinesia. If you increase the dose, the symptoms may temporarily be masked.9
Dr Trosch: I’ve often had patients who come to me with severe drug-induced parkinsonism, and I taper them off the neuroleptic. As I’m tapering them off and their parkinsonism is resolving, their tardive dyskinesia is unmasked. So I’m no longer treating them for drug-induced parkinsonism; now I’m treating them for tardive dyskinesia.
And they ask me, “Did taking me off the neuroleptic cause me to have tardive dyskinesia?” And I have to explain, “No, you had tardive dyskinesia. It was merely unmasked by removing the neuroleptic."
Dr Comella: And the opposite is the case with anticholinergics. In some cases, anticholinergics can worsen tardive dyskinesia, but they can improve drug-induced parkinsonism.9,10
Dr Trosch: Anticholinergics are not recommended for use in patients with tardive dyskinesia. I avoid this class of drugs in these patients.12
Dr Comella: That certainly makes sense.
Rich, as we wrap up, I want to underscore that we will need to be alert for signs of tardive dyskinesia, because it can affect patients both functionally and socially, and because it is treatable and potentially preventable if there is not an indication for a dopamine receptor blocking agent.10,13
Dr Trosch: And I’d add that, regardless of patient demographics or history, if a patient is on a neuroleptic, they are at risk for tardive dyskinesia.3 So all patients on a neuroleptic at any dose should be monitored closely in the same way. Because we have to catch tardive dyskinesia early and intervene.
Please explore the other resources available on this website for more detailed information on identifying and diagnosing tardive dyskinesia.
1. Fahn S, Jankovic J, Hallet M. The tardive syndromes: phenomenology, concepts on pathophysiology and treatment, and other neuroleptic-induced syndromes. In: Fahn S, Jankovic J, Hallet M, eds. Principles and Practice of Movement Disorders. 2nd ed. Saunders; 2011:415-446.
2. Lerner PP, Miodownik C, Lerner V. Tardive dyskinesia (syndrome): current concept and modern approaches to its management. Psychiatry Clin Neurosci. 2015;69(6):321-334.
3. Caroff SN, Citrome L, Meyer J, et al. A modified Delphi consensus study of the screening, diagnosis, and treatment of tardive dyskinesia. J Clin Psychiatry. 2020;81(2):19cs12983.
4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. American Psychiatric Association; 2013.
5. Savitt D, Jankovic J. Tardive syndromes. J Neurol Sci. 2018;389:35-42.
6. Tarsy D. Tardive dyskinesia. Curr Treat Options Neurol. 2000;2(3):205-214.
7. Prabhu SS, Almousa S, Fortier K, Reebye UN. Diagnosis of tardive dyskinesia in an oral surgical office. Clin Med Rev Case Rep. 2018;5(8):226.
8. Guy W. ECDEU Assessment Manual for Psychopharmacology: Revised. National Institute for Mental Health, Psychopharmacology Research Branch; 1976:534-537.
9. Ward MW, Citrome L. Antipsychotic-related movement disorders: drug-induced parkinsonism vs. tardive dyskinesia—key differences in pathophysiology and clinical management. Neurol Ther. 2018;7(2):233-248.
10. Tarsy D. Neuroleptic-induced extrapyramidal reactions: classification, description, and diagnosis. Clin Neuropharmacol. 1983;6(suppl 1):S9-S26.
11. Caroff SN, Hurford I, Lybrand J, Campbell EC. Movement disorders induced by antipsychotic drugs: implications of the CATIE schizophrenia trial. Neurol Clin. 2011;29(1):127-148, viii.
12. Benztropine mesylate [package insert]. Lake Forest, IL: Akorn; 2017.
13. McEvoy J, Gandhi SK, Rizio AA, et al. Effect of tardive dyskinesia on quality of life in patients with bipolar disorder, major depressive disorder, and schizophrenia. Qual Life Res. 2019;28(12):3303-3312.