Tardive Dyskinesia

•  Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications.
• Although they are associated with the use of neuroleptics, TDs apparently existed before the development of these agents.
• People with schizophrenia and other neuropsychiatric disorders are especially vulnerable to te development of TDs after exposure to conventional neuroleptics, anticholinergics, toxins, substances of abuse, and other agents.
• TDs are most common in patients with schizophrenia, schizoaffective disorder, or bipolar disorder who have been treated with antipsychotic medication for long periods, but they occasionally occur in other patients as well. For example, people with fetal syndrome, other developmental disabilities, and other brain disorders are vulnerable to the development of TDs,  even after receiving only 1 dose of the causative agent.
• TD has been associated with polymorphisms of  both the dopamine receptor D2 (DRD2) gene, 

TD has been associated with polymorphisms of both the dopamine receptor D2 (DRD2) gene, ^[1]  TaqI A and TaqI B and associated haplotypes, ^[2]  and of the dopamine receptor D3 (DRD3) gene, ^[1, 3]  the dopamine transporter (DAT) gene, and the manganese superoxide dismutase (MnSOD) gene.

Dysfunction of the dopamine transporter has been hypothesized to play a role in the development of TD. However, Lafuente et al did not find evidence of involvement of a polymorphism with a variable number of tandem repeats (VNTD) in the DAT gene (SLC6A3) in dyskinesias induced by antipsychotics. ^[4] Thus, further research is needed to investigate the role of the dopamine transporter in the development and maintenance of TD.