The exact etiology of tic disorder is not well understood, but a large number of medical studies strongly support the hypothesis of dopamine transmission disorder, and these studies have found: an increase in the amount of basal striatal and cortical dopamine receptors in the brain of patients with tic disorder; abnormal dopamine binding transport in the basal nucleus; higher dopamine release in children with agonists than in normal controls; and that drugs regulating dopamine metabolism, especially postsynaptic D2 receptor blockers are effective. Therefore, the main pairs of drugs currently available for the treatment of tic disorders are also directed at blocking dopamine receptors. Drugs such as thiopride, haloperidol, and atypical antipsychotics also have dopamine receptor blocking effects. In addition to dopamine transmitters, pentraxin, norepinephrine, glutamate, gamma amino butyric acid (GABA), cholinergic and opioid metabolism may also play a role in pathogenesis. There is growing evidence that these systems may interact together, particularly the dopamine and pentraxin systems. Some of the newer antitwitch drugs, such as aripiprazole, ziprasidone, and risperidone, work by acting on both receptors in a dual manner thereby enhancing efficacy.