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TD Workshop Introduction
From Overlooked to Identified: Bringing Tardive Dyskinesia Into Focus

Released: May 21, 2026

Jeremy Schreiber
Jeremy Schreiber, MSN, APRN, PMHNP-BC
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Key Takeaways
  • TD can be easy to miss but clinically consequential, so it is essential to monitor patients receiving antipsychotics or other dopamine receptor–blocking agents for subtle involuntary movements that may emerge gradually and progress over time.
  • TD is not just a movement disorder; it can disrupt daily life and treatment stability by contributing to embarrassment, stigma, social withdrawal, functional and occupational impairment, medical complications, and medication nonadherence that may increase relapse risk.
  • Early recognition and accurate differentiation from other drug-induced movement disorders provides the opportunity for timely treatment with FDA-approved VMAT2 inhibitors, reducing patient burden and improving quality of life.

Tardive dyskinesia (TD) was first described in the literature before mankind walked on the moon, yet we had no FDA-approved treatments for this condition until 2017.

TD is a chronic, often irreversible, movement disorder that most commonly develops due to prolonged exposure to dopamine receptor–blocking agents (DRBAs). The condition manifests as abnormal, involuntary movements that are characteristically choreiform (rapid, jerky, nonrepetitive), athetoid (slow, sinuous, continuous), or semirhythmic in nature. To be diagnosed as TD, these movements must persist for at least 4 weeks and follow at least 3 months of exposure to DRBAs (as little as 1 month of exposure in individuals 60 years of age or older).

Clinical Presentation
The most prominent manifestations of TD involve the orofacial region, with abnormal movements observed in the tongue, lips, jaw, and face in most affected individuals. These orofacial dyskinesias may appear as tongue darting, grimacing, chewing, sucking, or puckering movements. Approximately one half of patients experience limb involvement, and up to one quarter develop axial dyskinesia affecting the neck, shoulders, or trunk. TD can also affect other muscle groups, such as the pharyngeal, diaphragm, and abdominal muscles. A patient who develops TD movements in 1 body area is more likely to experience TD in other body regions as well. The onset is generally insidious in nature, with minimal to mild initial signs that gradually increase in severity. From a clinical perspective, this means it can often sneak up on us, escaping notice unless we are keen observers.

Etiology and Pathophysiology
TD results from chronic use of DRBAs, particularly antipsychotic medications, although nonpsychiatric medications such as metoclopramide also fall into this group. The pathogenesis remains incompletely understood, but evidence suggests involvement of dopamine receptor hypersensitivity or upregulation resulting from chronic dopamine receptor blockade, oxidative stress, and maladaptive synaptic plasticity.

Prevalence and Incidence
Estimates of the overall prevalence of TD in patients who have received long-term antipsychotic treatment range from 7.2% to 30%. Middle-aged or elderly individuals are more likely to develop TD, in part due to their potentially prolonged exposure to DRBAs.

Risk Factors
The most consistent and important risk factors for TD are older age and cumulative DRBA exposure time. Higher dosing (leading to greater cumulative drug exposure and receptor blockade) and development of other movement disorders are also consistently associated with TD risk. Additional risk factors include mood disorders (especially major depressive disorder), neurologic conditions, substance use disorders, diabetes mellitus, cognitive impairment, or neurologic deficits. First-generation antipsychotics carry a higher risk; risk is lower but still present with second-generation agents.

Burden and Impact
Although many may consider TD a cosmetic problem, it is often associated with significant distress and social avoidance. In addition, it may lead to serious medical complications such as ulcers in the cheeks and tongue, macroglossia, gait disturbance, postural instability, swallowing or breathing difficulties, muffled speech, weight loss, depression, and suicidal ideation. TD movements carry significant stigma and are associated with an overall poorer quality of life. Patients often have difficulty with work; absenteeism, reduced productivity, and overall work impairment are frequently reported. Finally, and perhaps of most importance, TD can lead to a lack of medication adherence and risk of relapse of the underlying condition; patients with TD may also skip medications for their underlying conditions, stop their antipsychotics, and even tell others not to take some psychiatric medications.

Differential Diagnosis and Identification
TD is a clinically distinct movement disorder. It is imperative to distinguish it from other movement disorders that may have confounding presentations, such as akathisia, dystonia, and drug-induced parkinsonism (DIP). Accurate differentiation between TD and DIP is particularly important because these conditions are thought to result from essentially opposite etiologies (increased dopamine signaling in TD vs decreased dopamine signaling in DIP), and thus misdiagnosis can lead to treatment that actually worsens symptoms. In addition, TD must be distinguished from withdrawal-emergent dyskinesia, which is typically time limited and will resolve without treatment. The 2020 APA Practice Guidelines for Patients with Schizophrenia recommend routine screening with a structured instrument such as the Abnormal Involuntary Movement Scale (AIMS) at regular intervals (timing determined by individual patient risk) and a clinical assessment for movement disorders at every visit. These guidelines apply not only to patients with schizophrenia but to all patients with any condition treated with antipsychotic medications.

Treatment
In 2017, vesicular monoamine transporter 2 (VMAT2) inhibitors became the first FDA-approved treatments for TD. These medications work by blocking VMAT2, the transporter responsible for packaging dopamine and other monoamines into presynaptic vesicles, reducing presynaptic dopamine release and subsequent dopamine signaling. Two VMAT2 inhibitors FDA-approved for TD, valbenazine and deutetrabenazine, have demonstrated efficacy in reducing TD symptoms in randomized controlled trials. Additional clinical trials have demonstrated positive impact of reduction in TD movements on patient-reported quality of life measures.

Summary
TD is often chronic and affects patients to a significant degree regardless of perceived severity. Fortunately, this condition is often responsive to treatment with FDA-approved agents, and the burden on patients can be greatly reduced if identified, correctly diagnosed, and treated.

Your Thoughts
What are your experiences assessing and treating TD in your patients?

Please join us on June 24, 2026, for an AAPA/ANCC-certified live virtual APP-focused workshop for an expert-led foundational TD education with guided practice, peer discussion, and reflection to enhance your diagnostic and management skills. A recording will also be made available after the live date for on-demand viewing.

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How confident are you in your ability to recognize and diagnose symptoms of TD in your patients?

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