Sensorimotor abnormalities in childhood onset psychotic disorders

项目概要/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群体中始终存在，并且也已被识别 作为一些有希望的幼儿期精神病危险因素之一。我们将采用组合 使用脑磁图（MEG）进行非侵入性神经影像的神经行为方法和 结构磁共振成像（MRI）。八十名患有儿童期精神病的年轻参与者 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 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。我们的将军 关于运动协调缺陷的观点有两个方面。首先，我们提出半球间的失败 运动抑制导致无法在双手协调中正确协调计时信号。第二，我们 相信从运动皮层到体感皮层的前馈传出复制机制的失败会导致 患者自身运动过程中的不正确的感知反馈。我们这项研究的长期目标是 完善精神障碍运动缺陷的神经生物学，为未来的家庭开发生物标志物 遗传风险研究并评估精神分裂症和情绪相关之间的神经生物学差异 精神病。其中一些生物标志物应该与精神病本身有关，而另一些则与精神病本身有关。 更多疾病特异性临床表现。这些知识可以 a) 有助于更早、更多地 准确的诊断，b) 改善发病时的治疗计划，c) 协助更准确的治疗 估计疾病轨迹和预后，d) 帮助开发可能的新内表型 e) 为未来有关遗传与发育的家庭研究奠定基础 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.