Tardive Dyskinesia Video Perspectives

Correll has been a consultant and/or advisor to or has received honoraria from AbbVie, Acadia, Alkermes, Allergan, Angelini, Aristo, Biogen, Boehringer-Ingelheim, Cardio Diagnostics, Cerevel, CNX Therapeutics, Compass Pathways, Darnitsa, Denovo, Gedeon Richter, Hikma, Holmusk, IntraCellular Therapies, Janssen/J&J, Karuna, LB Pharma, Lundbeck, MedAvante-ProPhase, MedInCell, Merck, Mindpax, Mitsubishi Tanabe Pharma, Mylan, Neurocrine, Neurelis, Newron, Noven, Novo Nordisk, Otsuka, Pharmabrain, PPD Biotech, Recordati, Relmada, Reviva, Rovi, Seqirus, SK Life Science, Sunovion, Sun Pharma, Supernus, Takeda, Teva, and Viatris. He provided expert testimony for Janssen and Otsuka. He served on a Data Safety Monitoring Board for Compass Pathways, Denovo, Lundbeck, Relmada, Reviva, Rovi, Sage, Supernus, Tolmar and Teva. He has received grant support from Janssen and Takeda. He received royalties from UpToDate and is also a stock option holder of Cardio Diagnostics, Mindpax, LB Pharma, PsiloSterics and Quantic.

May 25, 2023

3 min watch

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VIDEO: Modifiable, unmodifiable risk factors for tardive dyskinesia

Transcript

Editor’s note: This is an automatically generated transcript, which has been slightly edited for clarity. Please notify iwaters@healio.com if there are concerns regarding accuracy of the transcription.

There are various risk factors that predispose to tardive dyskinesia. We can basically separate them into the unmodifiable and the modifiable.

The unmodifiable have to do with knowing the risk group when you start a medication, or when you evaluate a patient. So, patient-related, and one of the most powerful risk factors is older age — age greater than 45 years. Also, female sex. And whether people are white or black, whereas patients of Asian origin have lower risk of tardive dyskinesia.

The other bucket of unmodifiable risk factors are illness-related — longer illness duration, intellectual disability and brain damage, negative symptoms in schizophrenia, mood disorders per se, cognitive symptoms in mood disorders, and also gene polymorphisms that involve dopamine signaling.

On the modifiable side, we have comorbidity-related risk factors like diabetes, smoking, alcohol and substance use, or baseline extrapyramidal symptoms, so we can do something about it. Treat the diabetes, have smoking cessation, and also instruct people to not use illicit substances or alcohol as much. And there are treatment-related ones that we have under control because we steer the treatment after discussing it and deciding it with the patient.

Does the patient really need a dopamine receptor blocker? Are there are alternatives if it's not psychosis? What about the cumulative high dose of plasma levels? So, we want to stay below the neuroleptic threshold. We don't want Parkinsonian side effects or akathisia; switch the treatment or lower the dose, and don't use anticholinergic treatment because that can make tardive dyskinesia worse, and it masks the underlying Parkinsonian symptoms that may be related to some internal damage. And finally, don't use first-generation antipsychotics that have the highest risk. Almost five-fold higher than the risk of tardive dyskinesia with second-generation agents.