Tardive dyskinesia (TD) is a severe side effect of antipsychotic treatment. Factors considered as predisposing include age, gender, emotional disorders, diabetes, development of EPS during early treatment, prolonged administration and use of high doses of conventional antipsychotics. The second generation antipsychotics are of significantly lower risk. Furthermore, there is evidence that they may have a therapeutic effect on TD. This is well established for clozapine and there are reports also for risperidone, olanzapine, quetiapine and amilsulpride. Aripiprazole inhibits central dopaminergic neuron activity by a partial agonistic effect on the presynaptic D2 dopamine autoreceptor and also acts as an antagonist at postsynaptic D2 dopamine receptors. Through this mechanism, aripiprazole exerts activity as a dopamine agonist in hypodopaminergic states, while acting as a dopamine antagonist when dopaminergic activity is increased. There is also evidence from basic science studies that aripiprazole causes little D2 receptor up-regulation.