Tardive Dyskinesia - Treatment
The most important step in the treatment of TD is prevention. Because TD is caused only by the use of DRAs, every effort should be made to limit the use of these drugs to those patients for whom no other treatment options are available. Physicians will continually review the patient's need for ongoing DRA therapy and examine patients who are receiving long-term treatment with DRAs at 3- to 6-month intervals for evidence of TD.
| Prevention of TD |
| Inform |
Weigh the risks of TD and benefits of treatment. Inform patients and their family members about these risks before instituting therapy with a DRA. |
| Restrict |
Restrict the use of DRAs to only those patients for whom no alternative treatment is available. |
| Limit |
Limit exposure by keeping the dose of DRA to the lowest possible level. |
| Assess |
Every three months, reassess the patient's need for continued treatment with a DRA. |
| Switch |
When possible, switch patients to a medication that has limited antagonism of dopamine receptors; for example, consider using an atypical antipsychotic rather than a typical antipsychotic drug. |
| Examine |
Every three months, examine patients who are taking DRAs for symptoms of TD. |
| Avoid |
Avoid the use of drug holidays; they have not been proven to be effective in reducing the risk of TD. |
The treatment of TD is challenging as the symptoms vary greatly among patients and because most patients with TD also have an underlying psychiatric illness, which necessitated the initial use of DRAs that caused the TD. This challenge is the delicate balance between the need for treatment of the essential psychiatric condition and the level of tolerable dyskinetic movements.
No pharmacologic treatment has been proven to be universally or even typically effective in the treatment of TD in clinical practice. Therefore, the treatment of TD is instead aimed at preventing, recognizing, and managing the movements. Discontinuing or reducing the level of the drug that caused the TD may lead to a reduction in the movements; however, the psychiatric illness may then be left untreated and become worse. When the use of a typical antipsychotic medication leads to TD, switching to an atypical antipsychotic medication may prove to be the most efficacious strategy.
Amine-depleting Drugs
Amine-depleting agents such as reserpine (Serpalan®, Serpasil®) and tetrabenazine (Nitoman) work on dopamine, norepinephrine, and serotonin; these drugs deplete the availability in the brain of these neurotransmitters. Few studies have been undertaken to evaluate the effectiveness of these drugs in the treatment of TD, although they are in widespread use in clinical practice. Tetrabenazine (Nitoman) appears to be the most effective drug for the treatment of TD, although it is not currently available in the United States. Amine-depleting agents seem to be most effective when not used at the same as neuroleptic therapy; instead, they may be used after the neuroleptic drug is stopped. Significant side effects limit the use of these drugs.
Branched-chain Amino Acids
A medical food comprising branched-chain amino acids (Tarvil™) seems to target excess phenylalanine. In clinical trials that studied adult men and adolescents as well as boys and girls with TD, the abnormal movements decreased significantly after the consumption of Tarvil™ three times a day. This treatment has few, if any, side effects.
Vitamin E
A 2000 Cochrane database review, which included a large clinical trial conducted by the Veterans Administration, found no or very limited evidence to support the use of vitamin E in the treatment of TD. In 2002, results of a 12-week clinical study were published (Zhang et al.) in which patients treated with an alpha-tocopherol (a specific form of vitamin E) had decreased scores on the Abnormal Involuntary Movement Scale and higher levels of superoxide dismutase, a measure of oxidative state.
