Exploring the functional, social, professional, and psychological impact of tardive dyskinesia movements on patients’ lives

TD is an underrecognized and typically misdiagnosed, drug-induced movement disorder^1–3

TD is an often irreversible extrapyramidal side effect (EPS) caused by long-term exposure to dopamine receptor-blocking agents (DRA).^1–3 The highest prevalence of TD has been reported among patients treated with antipsychotic medications, with approximately a quarter developing TD in their lifetime.^1,3 The involuntary arrhythmic movements of TD often affect the face; however, in some cases these extend to the trunk, limbs and extremities.^1,2,12,13 TD symptoms are chronic but may wax and wane in severity over time and have substantial impact on patients,  even when considered mild.^a,2,4,12 

TD affects daily functioning and well-being^5–7

The impact of TD movements on usual day-to-day activities, including eating and self-care can vary from 'a lot' to 'some' impact, but they frequently reduce quality of life.^5,6 Many patients with TD experience lower productivity and fewer are in full-time employment than those without TD.^5,6 They often feel uncomfortable in their own skin, with many feeling their ability to socialize is affected.⁵ Feelings of unacceptance and stigma may also develop as a result of discrimination by others.^6,7 For instance, when shown videos of actors simulating orofacial TD movements, approximately 50% of responders would not be "interested to meet in person for a coffee or a drink" or disagree that " the candidate would be suitable for client facing jobs".⁷ Patients with TD can also experience negative impacts on their psychological well-being and underlying psychiatric conditions.^4,5 Studies have found higher rates of EPS, drug or alcohol dependency, hospitalizations due to psychiatric conditions and reduced symptom remission in patients treated with antipsychotics with TD when compared with those without TD.^9,14 

TD is associated with reduced neurocognitive function^8,9

In some cases, TD may be associated with severe psychopathology and cognitive impairment.^8,9 When comparing patients with schizophrenia with and without TD, those with TD tend to score lower on neurocognitive tests reflecting functional ability in simple and complex tasks, attention and decision-making, processing speed, reasoning, and memory.^b,8,9

Early recognition is essential for the management of TD^2,12,13

TD presents in a similar way to other movement disorders, causing many patients to be misdiagnosed.^2,13 To prevent this happening, the American Psychiatric Association (APA) recommends that all patients treated with antipsychotic drugs are regularly assessed for movements associated with TD using a structured tool, such as the Abnormal Involuntary Movement Scale (AIMS).¹² The APA also recommends treatment with vesicular monoamine transporter 2 (VMAT2) inhibitors for anyone with moderate to severe or disabling TD. There are currently two FDA-approved VMAT2 inhibitors, deutetrabenazine and valbenazine.^c,10–12 These therapies do not require DRA withdrawal or dose modification, which can worsen underlying psychiatric conditions and trigger withdrawal-emergent dyskinesia.^10–12

^a_{Based on mental and physical health status evaluated using SF12v2 and SF-36v2 Health Survey scores. Scores range from 0–100, with higher scores indicating better health status;} ^b_{A neurocognitive composite score was calculated by creating a Z-score of the average of 5 standardized neurocognitive domain scores (verbal memory, working memory, processing speed, vigilance, and reasoning). Adjusted for baseline covariates;} ^c_{Please consult full prescribing information before use.}