Sensorimotor abnormalities in childhood onset psychotic disorders

项目摘要/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。运动障碍一直存在于精神病患者群体中，也已被确认 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 脑磁图无创神经成像的神经行为方法 结构磁共振成像(MRI)。80名患有儿童期起病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进行比较 受试者(N=40)，无精神病和/或双相情感障碍的个人或家族病史。我们的将军 对运动协调缺陷的看法有两个方面。首先，我们提出了半球间的故障 运动抑制导致在双手协调中正确协调计时信号的失败。第二，我们 相信从运动到躯体感觉皮质的前馈传出复制机制失败会导致 患者自身运动过程中的感知反馈不正确。我们这项研究的长期目标是 完善精神病患者运动障碍的神经生物学，开发未来以家庭为基础的生物标记物 精神分裂症与心境相关遗传风险的研究及神经生物学差异评价 精神病。这些生物标记物中的一些应该与精神病本身有关，而另一些与精神病本身有关 更具障碍特异性的临床表现。这样的知识可以a)有助于更早和更多地 准确的诊断，b)在发病时改进治疗计划，c)帮助更准确地 疾病轨迹和预后的估计，d)帮助可能的新的内表型的发展 精神病的标志物，以及e)形成未来关于遗传和发育的家庭研究的基础 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.