Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA; Minneapolis VA Health Care System, Minneapolis, MN, USA.
Department of Psychiatry, University of California San Diego, San Diego, CA, USA.
Psychiatry Res. 2019 Feb;272:135-140. doi: 10.1016/j.psychres.2018.12.007. Epub 2018 Dec 6.
There is accruing evidence of spontaneous dyskinesia in individuals with schizophrenia that is independent of medication exposure. Dyskinetic motor behavior is also present in individuals who are at high risk of schizophrenia and appears to have prognostic value for the development of psychosis. Nonetheless, it remains unclear whether dyskinesia is present in first-degree relatives of individuals with schizophrenia and thus associated with genetic liability for schizophrenia (i.e., an endophenotype), or whether the motor abnormality is a biomarker specific to the disease state spectrum. There is also limited information about links between dyskinesia and clinically relevant phenomena such as symptoms and cognition. Because dyskinesia marking genetic liability is likely to be subtle, we used sensitive instrument-based measurement of handwriting fluency to quantify dyskinesia in medicated individuals with schizophrenia or schizoaffective disorder, unaffected first-degree biological relatives of individuals with schizophrenia and schizoaffective disorder, and control participants. Results indicated that medicated individuals with schizophrenia or schizoaffective disorder exhibited more dyskinesia than both relatives and controls, with no difference between relatives and controls. Dyskinesia in individuals with schizophrenia or schizoaffective disorder was unrelated to current antipsychotic medication dosage, but associated with worse working memory function and greater positive formal thought disorder. These results provide evidence that dyskinesia is not associated with unexpressed genetic liability for schizophrenia.
越来越多的证据表明，精神分裂症患者存在与药物暴露无关的自发性运动障碍。高风险精神分裂症个体也存在运动障碍行为，且似乎对精神病的发展具有预后价值。尽管如此，运动障碍是否存在于精神分裂症患者的一级亲属中，从而与精神分裂症的遗传易感性（即内表型）相关，或者运动障碍是否是特定于疾病状态谱的生物标志物，仍不清楚。关于运动障碍与症状和认知等临床相关现象之间的联系，也只有有限的信息。由于运动障碍标记遗传易感性可能很微妙，我们使用基于仪器的敏感测量方法来衡量精神分裂症或分裂情感障碍患者用药后的书写流畅性，以量化精神分裂症患者或分裂情感障碍患者、未受影响的精神分裂症患者或分裂情感障碍患者的一级生物学亲属以及对照组参与者的运动障碍。结果表明，与亲属和对照组相比，精神分裂症或分裂情感障碍患者用药后的运动障碍更为明显，而亲属和对照组之间则没有差异。精神分裂症或分裂情感障碍患者的运动障碍与当前抗精神病药物剂量无关，但与较差的工作记忆功能和更大的阳性形式思维障碍有关。这些结果表明，运动障碍与精神分裂症的未表达遗传易感性无关。
