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MedCentralTardive Dyskinesia Medication Management

Understanding and Managing Tardive Dyskinesia: Pathophysiology, Prevention Strategies, and Evidence-Based Treatments

Tardive dyskinesia (TD) is a movement disorder primarily caused by long-term use of dopamine receptor antagonists, such as antipsychotic medications. Characterized by involuntary, rhythmic movements, TD significantly impacts patients’ quality of life. This article provides a comprehensive review of the current guidelines and evidence-based recommendations for the assessment, prevention, and management of TD, emphasizing practical implications for clinical practice.

Key Points:

  • Pathophysiology of TD:
    • TD is linked to increased sensitivity and the number of postsynaptic dopamine receptors due to long-term use of dopamine receptor antagonists.
    • Other hypotheses include oxidative stress affecting the basal ganglia and subcortex, and neurotransmitter imbalances involving GABA and NMDA receptors.
    • These theories guide current research and treatment strategies.
  • Prevention of TD:
    • Early prevention through the use of second-generation antipsychotics, which have a lower incidence of TD compared to first-generation antipsychotics.
    • Slow titration and use of the lowest effective dose to manage psychiatric disorders can help prevent TD.
    • Regular patient assessments and monitoring for TD every 6 months for first-generation and every 12 months for second-generation antipsychotics are recommended.
  • Screening Tools:
    • Abnormal Involuntary Movement Scale (AIMS): Most frequently used, clinician-rated 12-item scale for detecting and monitoring TD severity.
    • Dyskinesia Identification System Condensed User Scale (DISCUS): Clinician-rated 15-item scale for assessing and monitoring TD.
    • Extrapyramidal Symptom Rating Scale (ESRS): Clinician-rated 13-item scale for assessing TD and other drug-induced movement disorders.
    • Simpson-Angus Scale (SAS): Clinician-rated 10-item scale for screening parkinsonism and other extrapyramidal side effects.
  • Pharmacological Management:
    • Deutetrabenazine and Valbenazine: Both VMAT2 inhibitors received level A recommendations for TD treatment, with deutetrabenazine requiring twice-daily dosing and valbenazine offering once-daily dosing.
    • Amantadine: Level B recommendation; used adjunctively, showing significant reduction in AIMS scores.
    • Clonazepam: Limited evidence; not preferred due to potential for tolerance and adverse effects such as sedation and confusion.
    • Ginkgo Biloba: Level B recommendation; shows promise due to its antioxidant properties, with a relatively benign side effect profile.
    • Tetrabenazine: Limited evidence for TD, with a level C recommendation and a significant adverse effect profile.
  • Medication Adjustments:
    • Dose reductions, medication cessation, and cross-titration to second-generation antipsychotics are common strategies.
    • Increasing the dose of the current antipsychotic to mask TD symptoms is no longer recommended.
  • VMAT2 Inhibitors:
    • These medications reduce presynaptic dopamine levels without oversensitizing post-synaptic receptors.
    • Deutetrabenazine and valbenazine are preferred due to better efficacy and tolerability profiles compared to tetrabenazine.

Although an estimated two-thirds of individuals diagnosed with TD are unaware of their movements, the remaining one-third report being troubled by them and endorse emotional and physical distress. (PLoS One)

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