Pathophysiologic theories postulate that tardive dyskinesia arises from the development of chemical denervation supersensitivity of dopamine receptors produced by chronic long-term neuroleptic treatment. To test a dopamine receptor modification strategy, 16 patients with tardive dyskinesia were assigned to treatment with a neuroleptic plus bromocriptine (a dopamine agonist) or placebo for 10 weeks in a rising-dose design. Patients were evaluated weekly during the 10-week treatment period and for 8 weeks after medication withdrawal. No significant treatment effect was found in tardive dyskinesia response in the overall sample. When patients were classified by tardive dyskinesia subtype, patients with choreoathetoid symptoms exhibited only slight improvement with active treatment, which persisted after drug withdrawal; patients with dystonic symptoms showed moderate improvement that was drug and dose dependent. The sustained administration of substantial doses of a dopamine agonist did not produce significant adverse effects, including behavioral toxic effects. These results, although not statistically significant, are of clinical and heuristic interest.