Tardive dyskinesia is characterized by involuntary, repetitive, purposeless movements that can affect different parts of the body (1). It is strongly associated with a history of antipsychotic use and usually occurs after several years of treatment.

We report two cases in whom fluvoxamine was beneficial both depressive disorder and tardive dyskinesia.

The pathophysiology of tardive dyskinesia is complex and remains unclear. There is no definitive treatment for tardive dyskinesia, although tetrabenazine ameliorates tardive dyskinesia most effectively. Positron emission tomography showed that fluvoxamine bound to sigma-1 receptors in the living human brain at therapeutic doses, suggesting that sigma-1 receptors play a role in the mechanism of action of fluvoxamine.Currently, fluvoxamine was reported to be effective for both treating hemiballism and depression in a patient and it was suggested that fluvoxamine might act as a reducer of dopamine in striatal area (3). Similarly, the potent sigma-1 agonist fluvoxamine reduced dopaminergic activity in the striatal area in our case.

The potent sigma-1 agonist fluvoxamine might be an alternative treatment option for hyperkinetic movement disorders without significant side effects. More detailed, double-blind studies should clarify the potential use of fluvoxamine in the treatment of hyperkinetic movement disorders.