Sensorimotor abnormalities in childhood onset psychotic disorders

项目总结/摘要 我们请求支持一项关于儿童期精神病患者大脑感觉运动异常的研究 疾病。运动缺陷在精神病患者人群中一直存在， 作为少数几个有希望的儿童早期精神病风险因素之一。我们将采用以下组合： 使用脑磁图（MEG）的非侵入性神经成像的神经行为方法， 结构磁共振成像（MRI）。80名年轻的参与者， 双相情感障碍（N=40）或精神分裂症（N=40）将与年龄和性别匹配的比较进行比较 受试者（N=40）没有精神病和/或双相情感障碍的个人或家族史。我们的一般 运动协调缺陷的观点是双重的。首先，我们认为， 运动抑制导致在双手协调中不能正确地协调定时信号。二是 我认为，从运动皮层到体感皮层的前馈传出复制机制的失败导致了 患者自身运动过程中的不正确感知反馈。我们这项研究的长期目标是 完善精神障碍中运动缺陷的神经生物学，为未来基于家庭的 精神分裂症样和情绪相关的遗传风险和神经生物学差异的研究 精神病这些生物标志物中的一些应该与精神病本身有关，而另一些则与精神病本身有关。 更多的疾病特异性临床表现。这样的知识可以a）有助于更早和更多的 准确的诊断，B）导致改善疾病发作时的治疗计划，c）有助于更准确地 疾病轨迹和预后的估计，d）帮助开发可能的新的内表型 精神病的标志物，以及e）形成未来与遗传与发育相关的家庭研究的基础。 对这些疾病的贡献。

PROJECT SUMMARY/ABSTRACT We are requesting support for a study of brain sensorimotor abnormalities in childhood onset psychotic illnesses. Motor deficits are consistently found in psychotic patient populations and have also been identified as among a few promising early childhood risk factors for psychosis. We will employ a combination of neurobehavioral methods with non-invasive neuroimaging using magnetoencephalography (MEG) and structural magnetic resonance imaging (MRI). Eighty young participants with either childhood onset psychotic bipolar disorder (N=40) or schizophrenia (N=40) will be compared to age and gender matched comparison subjects (N=40) without personal or family history of psychotic and/or bipolar mood disorders. Our general perspective on motor coordination deficits is two-fold. First, we propose that a failure in inter-hemispheric motor inhibition results in failures to properly coordinate timing signals in bimanual coordination. Second, we believe that a failure in feed-forward efferent copy mechanisms from motor to somatosensory cortex results in improper perceptual feedback during patient's own movements. Our long term goals for this research are to refine the neurobiology of motor deficits in psychotic disorders, develop biomarkers for future family-based studies of genetic risk and evaluate neurobiological differences between schizophreniform and mood-related psychotic illnesses. Some of these biomarkers should be associated with psychosis per se and others with more disorder specific clinical manifestations. Such knowledge could a) contribute to earlier and more accurate diagnosis, b) lead to improved treatment planning at onset of illness, c) assist with more accurate estimate of illness trajectory and prognosis, d) aid in the development of possible new endophenotypic markers for psychosis, and e) form the basis for future family studies relating to genetic vs. developmental contributions to these disorders.