<unk>  was first described in the 1950s shortly after the introduction of chlorpromazine and other antipsychotic drugs. However, the exact mechanism of the disorder remains largely uncertain. The most compelling line of evidence suggests that<unk>  may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected. Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for<unk> . The D2 hypersensitivity hypothesis is also supported by evidence of a dose–response relationship, withdrawal effects, studies on D2 agonists and antagonists, animal studies, and genetic polymorphism research. Given similar doses of the same neuroleptic, differences among individuals still exist in the likelihood of developing<unk> . Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins. Decreased functional reserve or cognitive dysfunction, associated with aging, intellectual disability, alcohol and drug use, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics. Antipsychotic drugs can sometimes camouflage the signs of<unk>  from occurring in the early stages; this can happen from the individual having an increased dose of an antipsychotic drug. Often the symptoms of<unk>  are not apparent until the individual comes off of the antipsychotic drugs; however, when<unk>  worsens, the signs become visible. Other dopamine antagonists and antiemetics can cause<unk> , such as metoclopramide and promethazine, used to treat gastrointestinal disorders. Atypical antipsychotics are considered lower-risk for causing<unk>  than their typical counterparts with their relative rates of<unk>  of 13.1% and 32.4% respectively in short-term trials with haloperidol being the main typical antipsychotic utilised in said trials. Quetiapine and clozapine are considered the lowest risk agents for precipitating<unk> . From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, leading to<unk> . As of 2013, reports of<unk>  in aripiprazole have grown in number. The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the person more sensitive to<unk> . Since 1973 the use of these drugs has been found to be associated with the development of<unk> . Risk factors An increased risk of<unk>  has been associated with smoking in some studies, although a negative study does exist. There seems to be a cigarette smoke-exposure-dependent risk for<unk>  in people who are antipsychotic-treated . Elderly people are also at a heightened risk for developing<unk> , as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia.<unk>  is also more common in those that experience acute neurological side effects from antipsychotic drug treatment. Racial discrepancies in<unk>  rate also exist, with Africans and African Americans having higher rates of<unk>  after exposure to antipsychotics. Certain genetic risk factors for<unk>  have been identified including polymorphisms in the genes encoding the D3, 5-HT2A and 5-HT2C receptors.
Tardive dyskinesia
Akathisia
Focal dystonia
Torsion dystonia
Myoclonic dystonia
Paroxysmal dyskinesia
Pseudoathetosis
Dopamine-responsive dystonia