Tardive Dyskinesia.
Although there are many published studies on the treatment of tardive dyskinesia (TD), relatively few treatments have proven to be consistently useful in clinical practice. Reviewed critically, most treatments have produced only slight to moderate benefit in less than half the patients treated. Emphasis instead is on prevention, prompt detection, and management of early and potentially reversible cases. If a patient develops dyskinesia while taking an antipsychotic drug (APD), ideal management is immediate discontinuation of the APD, if this is psychiatrically feasible. The manifestations of TD should be documented and the patient examined to exclude other possible causes of dyskinesia. APDs should then be withheld in the hope that the dyskinesia will disappear. Although the dyskinesia may fade within several weeks, it has the potential to recur if APD treatment is reintroduced. Psychiatric reevaluation to consider alternative psychiatric diagnoses or treatments is strongly advised. If there is no alternative to reintroducing an APD for psychiatric treatment, then an atypical neuroleptic should be considered. Because dyskinesia is very often not disturbing enough to require treatment, the need for treatment of TD should be carefully assessed. For mild dyskinesia, low doses of a benzodiazepine (eg, clonazepam) may reduce the amount of both dyskinesia and associated anxiety. Anticholinergic drugs are unhelpful and may aggravate TD but, similar to their effect in idiopathic dystonia, may be effective in tardive dystonia. Botulinum toxin injections are of considerable value in managing localized forms of tardive dystonia, such as retrocollis or blepharospasm. Tetrabenazine and reserpine are presynaptic dopamine depletors that may have considerable efficacy in TD, especially tardive dystonia; however, their use is often limited by side effects. Based on the rationale that TD may be due to formation of free radicals, vitamin E has been used for treatment of TD, with mixed results. In some patients with persistent and disabling TD that fails to remit even after the patient is no longer taking an APD, it may be necessary to resume treatment eventually with a typical APD. This approach should be considered only as a last resort to suppress TD, however, because it carries the risk of preventing remission and possibly aggravating TD. In this case, further attempts to taper and discontinue the APD are recommended. At present, there is no evidence that established TD continues to progress in severity with continued APD exposure. This nonprogressive character of TD may provide to be a consolation to the patient and family and is also of potential medical-legal importance.
Tarsy
D
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. dtarsy@caregroup.harvard.edu