What is tardive dyskinesia?

What is Tardive Dyskinesia

Tardive dyskinesia (TD) is an involuntary movement disorder characterized by rapid, repetitive, purposeless movements—primarily affecting the orofacial region (mouth, lips, tongue) but potentially involving any body part—that develops as a consequence of long-term exposure to dopamine receptor-blocking agents, particularly antipsychotic medications. 1, 2

Clinical Characteristics

Movement Patterns

• The hallmark features are choreiform (dance-like) and athetoid (writhing) movements, not tremor 2
• Orofacial involvement is most common, manifesting as repetitive tongue protrusion, lip smacking, chewing movements, and facial grimacing 1, 3
• Movements can extend to the limbs and trunk, presenting as finger movements, toe tapping, or truncal rocking 3, 4
• The movements are involuntary, stereotypical, and persist throughout waking hours 5

Distinguishing Features

• TD involves rapid involuntary facial and extremity movements focusing on choreiform and athetoid patterns—if tremor is the primary feature, consider drug-induced parkinsonism instead 2
• Unlike acute dystonic reactions, TD develops late in the course of treatment (hence "tardive" meaning delayed) 3
• The movements are out of the patient's control and can be socially embarrassing and physically disabling 4, 6

Etiology and Risk Factors

Causative Agents

• Any dopamine receptor-blocking agent can cause TD, including typical and atypical antipsychotics, as well as medications used for nausea or gastrointestinal dysfunction 3
• Atypical antipsychotics carry lower risk compared to typical antipsychotics 1, 7

High-Risk Populations

• Up to 50% of youth receiving neuroleptics may experience some form of tardive or withdrawal dyskinesia 1, 7
• Elderly patients have substantially higher rates than the general population 3
• Female sex, affective disorders, and patients without psychotic diagnoses are at increased risk 3
• Total cumulative drug exposure is positively correlated with TD risk 3

Prevalence

• Overall prevalence ranges from 0.5% to 56%, with mean reported prevalence of 15% in institutionalized patients 4
• Current estimates suggest 20-30% of hospitalized psychiatric patients in some populations develop TD 8

Pathophysiology

The underlying mechanism likely involves altered dopaminergic function, though the exact pathogenesis remains unproven 3, 4. The prevailing theory suggests chronic dopamine receptor blockade leads to compensatory receptor upregulation and hypersensitivity 4.

Clinical Significance and Prognosis

Persistence and Reversibility

• TD is potentially irreversible—it may persist even after medication discontinuation 1, 7, 3
• The risk of permanence increases with longer duration before detection 6
• Favorable outcomes (improvement or resolution) correlate with younger age, early detection, lower drug exposure, and longer follow-up duration 3

Impact on Quality of Life

• The movements are socially embarrassing and can produce significant disability 4
• Physical and psychological effects can be serious due to the uncontrollable nature of movements 6

Assessment

Baseline assessment of abnormal movements should be recorded before starting antipsychotic therapy using standardized measures like the Abnormal Involuntary Movement Scale (AIMS) 1, 7. The AIMS assesses involuntary movements across seven body regions on a 0-4 scale, with total scores ranging from 0-28 9.

Regular monitoring for dyskinesias should occur at least every 3-6 months using the AIMS 1, 7, as early detection is crucial for better outcomes 1, 7, 6.