Fast Five Quiz: How Much Do You Know About Tardive Dyskinesia?

Matthew Swan, MD

Disclosures

April 30, 2019

Two central monoamine-depleting agents, deutetrabenazine and valbenazine, have recently been approved to treat TD. These selective vesicular monoamine transporter 2 (VMAT2) inhibitors modulate presynaptic packaging and release of dopamine into the synapse.

Unless a patient is suffering from a life-threatening condition such as neuroleptic malignant syndrome, the dopamine antagonist dosage should be tapered slowly, usually by 10% increments of the original dose, while monitoring for reemergence or worsening of psychotic symptoms. Abrupt cessation of dopamine antagonists can provoke florid psychosis with hallucinations, delusions, and homicidal or suicidal behavior. For patients with TD, some clinicians continue or increase the dose of antipsychotic medication, which can improve symptoms; however, this strategy is controversial because it may require ongoing dose escalation. This can increase the risk for side effects such as weight gain, sedation, and metabolic syndrome.

Although some studies indicate that second-generation (atypical) antipsychotic drugs (eg, aripiprazole) may have a beneficial effect on TD remission, the role of these drugs in TD remission is controversial. Moreover, second-generation neuroleptic drugs may alleviate symptoms of TD, as previously noted, but they can also trigger TD. Therefore, based on current data, these drugs are generally not recommended in the treatment of TD. Although there is anecdotal support for botulinum toxins in treating TD, there is an overall paucity of good-quality evidence. Current guidelines suggest that there is insufficient evidence to support or refute the use of botulinum toxins for treating PD.

For more on treatment options for TD, read here.

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