Deutetrabenazine and valbenazine are selective vesicular monoamine transporter 2 (VMAT2) inhibitors that decrease presynaptic dopamine and are the treatment of choice for TD. In addition, in some patients, such as patients with schizophrenia, discontinuation of antipsychotic therapy is not an option due to the risk for relapse; VMAT2 inhibitors may be useful in controlling TD symptoms without modifying the antipsychotic medications.
If clinically feasible, management of TD includes the withdrawal of the antipsychotic medication. However, the dosage should be tapered slowly, while monitoring for reemergence or worsening of psychotic symptoms. Abrupt cessation of dopamine antagonists can provoke psychosis with hallucinations, delusions, homicidal or suicidal behavior, and withdrawal dyskinesia.
Although the risk for TD is significantly lower with second-generation antipsychotics (SGA) compared with first-generation antipsychotics (FGA), all antipsychotics are associated with the development of TD. Switching to an SGA with lower affinity to D2 receptors, such as clozapine or quetiapine, may reduce TD symptoms; however, improvement in symptoms may take up to a few years to occur.
There is little evidence to support the use of botulinum toxin in the treatment of tardive dyskinesia. However, it may be useful in patients with tardive dystonia.
Learn more about treatment options for TD.
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Cite this: Matthew Swan, James Robert Brasic. Fast Five Quiz: How Much Do You Know About Tardive Dyskinesia? - Medscape - Apr 22, 2022.