Tardive Dyskinesia – Examination and Management
Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients with long-term exposure to antipsychotics.
Tardive dyskinesia occurs due to supersensitivity of dopamine (D2) receptors after long-term exposure to antipsychotics resulting in downregulation of D2 receptors.
The Abnormal Involuntary Movement Scale (AIMS) is commonly used to quantify the severity of TD and should be considered as a regular and routine part of clinical management. See below.
Tardive dyskinesia is also known to occur in neuroleptic-naive individuals which may indicate the underlying pathophysiology of the illness.
Alcohol abuse, smoking, diabetes mellitus, organic neurological impairment, female sex, typical antipsychotics and affective disorders may increase the risk of TD.
Prevention is paramount: Select an antipsychotic with lower propensity for TD
Address smoking (Risk factor for TD)
Reduce dose of antipsychotic. (In some cases this can worsen dyskinetic movements)
Change to atypical drug if on typical antipsychotic.
If untreated; consider switch to Clozapine
Other strategies include:
- Tetrabenazine – depressogenic, useful in Huntington’s
- Vitamin E
Latest: Valbenazine is a novel, highly selective vesicular monoamine transporter 2 inhibitor that has recently been approved by the FDA for the treatment of Tardive Dyskinesia. Once-daily valbenazine significantly improved tardive dyskinesia in participants with underlying schizophrenia, schizoaffective disorder, or mood disorder at doses of 80 mg/day.