Abstract
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Extrapyramidal motor side effects (EPMS) are major side effects of neuroleptic treatment. Like in tardive dyskinesia there is evidence for a genetic predisposition in developing early dyskinesia (ED). Since most neuroleptics inhibit dopamine D2-like receptors, such as DRD3, it is reasonable to assume a contribution of these receptor variants to the vulnerability for the development of ED. A comparison of the Ball polymorphism in the dopamine DS-receptor was carried out between schizophrenic patients with (n = 78) and without (n = 72) ED under equal standardized neuroleptic medication. Regarding the 2-2 genotype versus non 2-2, we found a significant higher frequency of homozygosity for allele 2 in patients suffering from ED compared to patients without ED (Fisher Exact Test, two sided; P = 0.035). Our data indicate that homozygosity for the Ball allele of the DRD3 gene is a risk factor for the development of ED. These results are in line with previous results, showing a close correlation between the DRD3 Ball polymorphism and the development of tardive dyskinesia.