Spatial frequency contributions to contour integration deficits in schizophrenia

项目总结/摘要 轮廓整合（CI）-对于本申请的目的-指的是在空间上表示 分离的边缘作为单个连续轮廓。大量研究表明精神分裂症患者 (SZ)轮廓整合受损，但机制，时程，和临床意义的 才刚刚开始探索这些缺陷。为了阐明这一问题，我们进行了两个阶段的 心理物理调查在第一阶段，我们将满足NIMH策略1.1，并阐明神经网络 赤字背后的机制（目标1）。迄今为止的临床CI研究几乎完全采用了较低的 空间频率轮廓元素（<7周/度），但收敛的证据表明，精神分裂症是 其特征在于大细胞功能障碍，相应地，低空间的加工受损， 频率（<8个周期度）。为了确定空间频率处理是否可以解释CI缺陷， SZ、晚发患者组和匹配的健康对照组将执行4项不同的任务。的 每个任务的刺激的空间频率结构将有所不同，包括或不包括低空间 频率.如果CI缺陷出现，甚至与高空间频率定义的元素，那么受损的横向 早期视觉皮层的相互作用将被证明是精神分裂症的核心特征。如果CI 只有当较低的空间频率可用时，功能障碍才会出现，那么这将增加日益增长的 SZ中大细胞功能障碍的证据，并将提供一个新的解释结果源于 CI任务。在第二个数据收集阶段，我们将满足NIMH战略2.1，并检查 从第一次发作开始的CI缺陷（目标2）。新招募的受试者将是健康对照，首先- 发作患者或后期发作患者。第二阶段的任务将与 在第一阶段显示组间差异（p<0.05）。重要的是，这一阶段将提供第一个 最近经历过第一次精神分裂症的精神分裂症患者中是否存在CI缺陷的数据 精神病发作在数据收集结束时，我们将跨阶段联合收割机数据合并为两个 决心。首先，我们将评估CI缺陷-在高或低空间频率-是否与以下因素相关： 临床变量，如：功能结局、紊乱症状、阳性/阴性症状，以及 病前社会功能（目标3）。第二，我们将比较四个任务的基础上： 效应量、预测疾病特征的能力、总持续时间和脱落率（目标4）。评估任务 这将指导未来更大规模的研究，旨在进一步建立，解释，或利用轮廓 精神分裂症的缺陷总之，在两个数据收集阶段实现的四个目标将阐明 轮廓整合功能障碍的神经机制、时程、临床相关因素和最佳测量方法 精神分裂症

Project Summary/Abstract Contour integration (CI)-for the purposes of the present application-refers to the ability to represent spatially segregated edges as a single continuous contour. Numerous studies suggest that people with schizophrenia (SZ) are impaired at contour integration, but the mechanisms, time-course, and clinical implications of the impairment are just beginning to be explored. To shed light on this issue, we conduct a two phase psychophysical investigation. In the first phase, we will satisfy NIMH Strategy 1.1, and clarify the neural mechanisms behind the deficit (Aim 1). Clinical CI studies to date have almost exclusively employed lower spatial frequency contour elements (<7 cycles/deg), but converging evidence suggests that schizophrenia is characterized by magnocellular dysfunction and, correspondingly, impaired processing of lower spatial frequencies (<8 cycles deg). To determine whether spatial frequency processing can account for CI deficits in SZ, a later-episode patient group and a matched healthy control group will perform 4 different tasks. The spatial frequency structure of the stimuli for each task will be varied to either include or not include low spatial frequencies. If CI deficits arise even with elements defined by high spatial frequencies, then impaired lateral interactions in early visual cortex would be evidenced as a core feature of schizophrenia. By contrast, if CI dysfunction arises only when lower spatial frequencies are available, then that would add to the growing evidence for magnocellular dysfunction in SZ, and would provide a new interpretation of results stemming from CI tasks. In the second data collection phase, we will satisfy NIMH Strategy 2.1 and examine the development of CI deficits from first-episode onward (Aim 2). Newly recruited subjects will be either healthy controls, first- episode patients, or later-episode patients. The tasks in this second phase will be the same as those that revealed between-group differences (p<0.05) in the first phase. Importantly, this phase will provide the first data on whether CI deficits exist among people with schizophrenia who recently experienced their first psychotic episode. At the end of data collection, we will combine data across phases to make two determinations. First, we will assess if CI deficits-at either high or lower spatial frequencies- correlate with clinical variables such as: functional outcome, disorganized symptoms, positive/negative symptoms, and premorbid social functioning (Aim 3). Second, we will compare the four tasks on the basis of: between-group effect sizes, capacities to predict illness features, total duration, and drop-out rate (Aim 4). Evaluating the tasks in this way will guide future larger-scale studies aiming to further establish, explain, or make use of contour deficits in schizophrenia. In summary, the four aims achieved over two data collection phases will elucidate the neural mechanisms, time course, clinical correlates, and optimal measures of contour integration dysfunction in schizophrenia.