What is dyskinesia?

Dyskinesia: Definition and Clinical Manifestations

Dyskinesia is a neurological disorder characterized by involuntary, abnormal, irregular, and purposeless movements that can affect various body regions, most commonly the orofacial area but potentially involving any body part.1, 2

Types of Dyskinesia

• Tardive Dyskinesia (TD): The most common form, associated with long-term use of dopamine receptor-blocking agents (primarily antipsychotics), characterized by choreoathetoid movements typically affecting the orofacial region, limbs, and trunk 1, 3

• Paroxysmal Kinesigenic Dyskinesia (PKD): Characterized by recurrent and transient attacks of involuntary movements (dystonia, chorea, ballism) precipitated by sudden voluntary actions, with episodes typically lasting less than 1 minute 4, 5

• Paroxysmal Non-Kinesigenic Dyskinesia (PNKD): Involves involuntary movements that cannot be triggered by movement, occur less frequently than PKD but last longer 5

• Levodopa-induced Dyskinesia: Commonly seen in Parkinson's disease patients receiving long-term levodopa therapy 6

Clinical Manifestations

• Movement Types: Dyskinesias can manifest as:

  • Dystonia (sustained muscle contractions causing twisting movements)
  • Chorea (brief, irregular, dance-like movements)
  • Ballism (large amplitude, flinging movements)
  • Athetosis (slow, writhing movements) 4, 3

• Body Distribution:

  • Tardive dyskinesia typically affects the orofacial region (70% of patients), causing facial twitching, rigidity of facial muscles, and dysarthria 4
  • Can also involve the limbs and trunk 3
  • In PKD, face involvement is reported in approximately 70% of patients 4

• Duration and Frequency:

  • PKD attacks typically last less than 1 minute in over 98% of patients 4
  • PKD attack frequency varies significantly among individuals, ranging from several times a year to more than 100 times per day 4

Risk Factors for Tardive Dyskinesia

• Medication-related: Long-term use of dopamine receptor-blocking agents, particularly first-generation antipsychotics 1, 7

• Patient-related:

  • Advanced age (elderly patients at higher risk)
  • Female sex
  • Affective disorders
  • Patients without psychotic diagnoses receiving antidopaminergic drugs for non-psychiatric conditions 3

• Treatment-related: Total drug exposure positively correlates with TD risk 3

Pathophysiology

• While not fully understood, altered dopaminergic function plays a central role in the development of dyskinesias 3

• In tardive dyskinesia, prolonged blockade of dopamine receptors may lead to receptor hypersensitivity 2

• PKD is often associated with genetic abnormalities, with proline-rich transmembrane protein 2 (PRRT2) identified as the first causative gene 4

Management Approaches

• For Tardive Dyskinesia:

  • If clinically feasible, gradually withdraw the offending antipsychotic medication 1, 8
  • Consider switching to atypical antipsychotics with lower D2 affinity when antipsychotic treatment must continue 1, 8
  • FDA-approved medications include valbenazine and deutetrabenazine, which have demonstrated efficacy in reducing TD symptoms 9, 10, 9

• For PKD:

  • Anticonvulsants are highly effective for PKD 5
  • Some patients can alleviate attacks by slowing their movements when experiencing aura 4

Prevention and Monitoring

• Baseline assessment of abnormal movements before starting antipsychotic therapy 1, 8

• Regular monitoring using standardized measures like the Abnormal Involuntary Movement Scale (AIMS) every 3-6 months 1, 8

• Early detection is crucial as tardive dyskinesia may persist even after medication discontinuation 1, 8

Special Considerations

• The concern over dyskinesia risk should be balanced against the potential benefits of necessary medications 1, 8

• Adequate informed consent regarding dyskinesia risk is necessary when prescribing medications with potential to cause movement disorders 1, 11