Physician’s Weekly interviews Joseph McEvoy, MD, Professor Emeritus of Psychiatry and Behavioral Sciences, at Duke University School of Medicine, and Jonathan Meyer, MD, Clinical Professor of Psychiatry at University of California, San Diego, and a Psychopharmacology Consultant for California State Department of Health, about the basics of tardive dyskinesia.
Joseph McEvoy, MD, of Augusta University in Georgia and Duke University Medical Center in Durham, North Carolina
Jonathan Meyer, MD, Clinical Professor of Psychiatry, University of California San Diego
PW: What is the clinical definition of tardive dyskinesia (TD)?
Dr. McEvoy: The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) defines tardive dyskinesia (TD) as “involuntary athetoid or choreiform movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles) developing in association with the use of a neuroleptic medication for at least a few months.”1
PW: What are the symptoms of TD?
Dr. McEvoy: As summarized in the DSM-5, TD is characterized by abnormal and involuntary movements, often in the orofacial region (tongue, lips, facial muscles, jaw) but also in the upper extremities (arms, hands, fingers), lower extremities (legs, feet, toes), and trunk.2-4 These movements have been described as choreiform (irregular, dance-like) and athetoid (slow, writhing).4 Although assessing and reducing the severity of TD symptoms is crucial for clinical management, it is important to note that impact on patients (e.g., impaired physical and social function, embarrassment) can significantly reduce quality of life for both patients and their caregivers.5 For example, highly functioning patients who are aware of their symptoms (e.g., those with mood disorders) may be very bothered by their TD movements, even if those movements are “mild” in terms of amplitude and frequency.
PW: What is the difference between orofacial dyskinesia or oro-bucco-lingual dyskinesia?
Dr. McEvoy: Oral-buccal-lingual dyskinesia is the repetitive, chewing movement of the mouth and/or jaw, often with tongue protrusion and lip pursing or smacking, which is considered to be the “classic” manifestations of TD. Oral‑buccal-lingual dyskinesia accounts for many TD cases and can lead to difficulty speaking, swallowing, and eating, lip/tongue biting, and the cracking or grinding down of teeth.4 Orofacial dyskinesia includes oral-buccal-lingual movements of the mouth/jaw, as well as irregular facial movements (e.g., grimacing) and increased eye blinking or blepharospasm.4
PW: What other parts of the body can be affected by TD?
Dr. McEvoy: TD may also present in the upper extremities as “piano-playing” movements of the fingers/hands, in the lower extremities as tapping of the toes/feet, or in the neck or trunk as rocking or thrusting. In severe cases, balance and/or ambulation can be impaired by excessive movements in the arms, legs, or trunk.4 In milder cases, TD may not be easily apparent during the visual assessment (e.g., toe or foot tapping may not be visible if patient’s feet are covered by shoes/socks). In addition, some patients may not be aware of their abnormal movements due to cognitive impairment from underlying severe schizophrenia, while others may not report TD symptoms due to embarrassment or greater concern with other medical or psychiatric conditions.4 Therefore, caregivers and/or family members should be encouraged to participate in the patient’s assessments, as they can provide useful information about the location and severity of any abnormal movements, as well as the impact of those movements on the patient’s functioning and quality of life.
PW: What are the causes and risk factors for TD?
Dr. Meyer: The major cause of TD is exposure to a dopamine-receptor blocking agent (DRBA). This class includes first- and second-generation antipsychotics (FGAs, SGAs), the motility agent metoclopramide, and chronic exposure to weak dopamine antagonists used as antiemetics (e.g. prochlorperazine). With the expanding use of SGAs, the number of patients at risk for TD continues to rise. In addition to the treatment of schizophrenia, SGAs are approved for mood disorders (e.g., bipolar mania or bipolar depression, unipolar major depression, Tourette’s disorder, irritability associated with Autistic disorder) and are often used off‑label for behavioral issues (e.g., agitation, irritability, aggression) in individuals with psychiatric, neuropsychiatric, or neurodevelopmental disorders (e.g., dementia, intellectual disability).6-8 SGAs are less likely to cause TD than FGAs, but evidence indicates that the risk associated with both classes is substantial. In a 2017 meta-analysis, the prevalence of TD was 30% in patients receiving FGAs and 21% for SGAs; in FGA-naïve patients who had only received SGAs, the prevalence was still 7%.9 According to DSM-5, TD usually develops after at least a few months of antipsychotic treatment, or even sooner in older patients.1 The risk of TD increases with longer treatment, but in some patients TD can appear within weeks or even days.10
In addition to DRBA exposure, studies have shown that older age is the greatest source of risk for TD, with incidence rates 5-fold greater than those among younger patients.11 Additional potential risk factors are female sex, psychiatric diagnosis, higher ratings of negative symptoms in schizophrenia, greater cognitive impairment, diabetes, substance abuse, and prior adverse reaction to DRBAs (e.g., parkinsonism, akathisia, dystonia, or treatment- or withdrawal-emergent dyskinesia).11,12
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