Tardive dyskinesia (TD) is a serious, often disabling, movement disorder that is 
caused by medications that block dopamine receptors (i.e., neuroleptics, 
anti-emetics). There is currently no standard treatment approach for physicians 
confronted with such patients. This may be the result of notions that TD is 
disappearing because of the switch to second-generation antipsychotic agents and 
that it is largely reversible. In this article we demonstrate that 
second-generation antipsychotics do, indeed, cause TD and, in fact, the 
frequency is likely higher than expected because of growing off-label uses and a 
tripling of prescriptions written in the last 10 years. In addition, studies 
demonstrate that TD actually remits in only a minority of patients when these 
drugs are withdrawn. Furthermore, neuroleptic agents are often utilized to treat 
TD, despite prolonged exposure being a risk factor for irreversibility. The 
outcome of these trends is a growing population afflicted with TD. We review 
non-neuroleptic agents that have shown positive results in small, early-phase, 
blinded trials, including tetrabenazine, amantadine, levetiracetam, piracetam, 
clonazepam, propranolol, vitamin B6, and Ginkgo biloba. Other options, such as 
botulinum toxin and deep brain stimulation, will also be discussed, and a 
suggested treatment algorithm is provided. While these agents are reasonable 
treatment options at this time there is a need, with a concerted effort between 
neurology and psychiatry, for full-scale drug development, including 
multicenter, randomized, blinded trials to confirm the effectiveness of the 
agents that were positive in phase 2 trials and the development of newer ones.