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

Matthew Swan, MD


May 21, 2021

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. If discontinuing use of the agent poses too great of a risk, VMAT2 inhibitors may be useful in controlling TD symptoms without modifying the antipsychotic medications, thereby curbing hospital admissions.

Clonazepam, 0.25-4 mg per day, is probably effective for the treatment of TD by increasing gamma amino butyric acid (GABA) neurotransmission and thus reducing dopamine neurotransmission.

Gingko biloba, 80-240 mg per day, is probably effective for the treatment of TD through antioxidant effects.

Amantadine, 100-300 mg per day, is possibly effective for the treatment of TD. Clinicians must monitor for cognitive impairment and hallucinations. Vaidyanathan and Jaiswal also provide scientific evidence for clonazepam, gingko biloba, and amantadine as effective treatments.

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.

The transition from first-generation to second-generation (atypical) antipsychotic drugs (eg, aripiprazole) is thought to have reduced, but not eliminated, the risk of developing TD. Although some studies indicate that they may actually 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.

Learn more about treatment options for TD.


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