Perceptual Mechanisms of Visual Hallucinations and Illusions in Psychosis

精神病视幻觉和幻觉的知觉机制

• 批准号: 9448446
• 负责人: Scott R Sponheim
• 金额: $ 51.32万
• 依托单位: UNIVERSITY OF MINNESOTA
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-09-21 至 2022-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9448446
• 关键词: Anterior; Architecture; Attention; Behavior; Behavioral; Biological; Brain; Brain region; Complex; Computer Simulation; Cues; Data; Detection; Development; Discrimination; Elements; Exhibits; Failure; Form Perception; Frequencies; Functional Magnetic Resonance Imaging; Gaussian model; Genetic; Goals; Hallucinations; Illusions; Impairment; Individual; Intervention; Knowledge; Laboratories; Lead; Link; Location; Magnetoencephalography; Maps; Mental disorders; Modeling; Patient Self-Report; Perception; Performance; Physiology; Prefrontal Cortex; Process; Psychopathology; Psychophysics; Psychotic Disorders; Publishing; Regulation; Research Personnel; Siblings; Signal Transduction; Source; Task Performances; Techniques; Testing; Variant; Vision; Visual; Visual Cortex; Visual Hallucination; Visual Illusions; Visual Perception; Work; base; brain abnormalities; deviant; experience; extrastriate visual cortex; frontal lobe; insight; neural circuit; neuroimaging; neuromechanism; relating to nervous system; response; symptomatology; visual processing

Project Summary It is unknown how functions of the brain give rise to psychotic experiences in severe psychopathology. Consequently, available treatments for psychotic disorders are often marginally effective. Abnormal visual perception is evident in psychosis (e.g., hallucinations) and noted in people with genetic liability for psychotic psychopathology (e.g., heightened illusions). Current evidence points to early visual abnormalities in psychosis that may trigger a cascade of errant neural activity creating distortions in one's visual experience; however, it is unclear how basic visual and complex guidance functions of the brain separately contribute to visual misperception in psychotic psychopathology. The overarching goal of the proposed work is to use sophisticated psychophysical tasks and neuroimaging to a) precisely characterize behavioral and neural abnormalities in individuals with psychotic disorders during visual perception, b) detail the mechanisms of visual hallucinations and distortions through the development and testing of a computational model c) determine if the mechanistic anomalies also mark genetic liability for psychosis. The goal will be accomplished by studying individuals with psychotic disorders (IPDs), one first-degree biological sibling of each IPD (SibIPDs), and healthy controls (HCs) demographically similar to the other two groups. We hypothesize that individuals prone to visual hallucinations exhibit stable neural abnormalities in early visual cortex (V1, V2) causing errors in the processing of visual elements, and that visual hallucinations occur in IPDs when contextual influences of more anterior regions (LOC/fusiform, prefrontal cortex) on visual perception become deviant. Individuals prone to anomalous visual illusions but without a psychotic disorder are hypothesized to exhibit a stable decrement in high-level influences on visual perception reflected in anomalies of inter-regional neural synchronization. We will employ contrast discrimination, surround suppression, attention regulation, and ambiguous object tasks to assess early visual perceptual processes, with and without contextual modulation, in IPDs, their unaffected biological siblings (SibIPDs), and healthy controls (HCs), to determine when task performance predicts self-reported visual misperceptions. We will compute cortical source signals from 248-channel MEG data functionally localized through 7 Tesla (T) fMRI to detail the location, timing, and synchronization of neural responses during visual perceptual tasks assessing local and long-range processes in IPDs, SibIPDs, and HCs, as well as determine how neural responses elicited by tasks predict variation in self-reported visual misperception. We will also characterize visual responses in all tasks using the Gaussian Scale Mixture model originally published by Schwartz et al (2009) and recently extended in our work to generalize across multiple scene segmentation cues (Qiu, 2013). We will use this model to test whether terms reflecting local inhibition are selectively reduced in all IPDs and whether the strength of the term representing long-range modulation correlates with frequency of visual hallucinations.

项目摘要 在严重的精神病理学中，大脑的功能是如何引起精神病经历的，这是未知的。 因此，现有的治疗精神障碍的方法往往是边际有效的。异常视觉 感知在精神病中是明显的（例如，幻觉），并指出，在人与遗传倾向的精神病 精神病理学（例如，增强的幻觉）。目前的证据表明精神病的早期视觉异常 这可能会引发一连串的错误神经活动，在一个人的视觉体验中造成扭曲;然而， 不清楚大脑的基本视觉功能和复杂的指导功能如何分别对视觉产生影响。 在精神病心理病理学中的误解拟议工作的总体目标是利用 复杂的心理物理任务和神经成像，以a）精确表征行为和神经 在视觉感知过程中精神病患者的异常，B）详细说明了 c）通过开发和测试计算模型来消除视觉幻觉和扭曲 确定机械异常是否也标志着精神病的遗传倾向。 这一目标将通过研究患有精神障碍（IPD）的个体来实现， 每种IPD的生物学同胞（SibIPD）和与其他两种IPD在人口统计学上相似的健康对照（HC） 组我们假设，有幻视倾向的个体在大脑中表现出稳定的神经异常， 早期视觉皮层（V1，V2）导致视觉元素处理错误， 当更前部的区域（前额叶/梭形，前额叶皮层）对视觉的背景影响时， 感知变得异常。有异常视错觉倾向但没有精神障碍的人， 假设在异常中反映的视觉感知的高水平影响中表现出稳定的递减 区域间的神经同步我们将使用对比度辨别，环绕声抑制， 注意力调节和模糊物体任务，以评估早期视觉感知过程，有和没有 在IPD、其未受影响的生物同胞（SibIPD）和健康对照（HC）中， 确定任务表现何时预测自我报告的视觉错觉。我们将计算大脑皮层 通过7特斯拉（T）fMRI功能定位的248通道MEG数据源信号，以详细说明 在视觉感知任务中评估局部和 在IPD，SibIPD和HC中的长程过程，以及确定任务如何引起神经反应 预测自我报告的视觉错觉的变化。我们还将描述所有任务中的视觉反应 使用最初由Schwartz等人（2009年）发表的高斯尺度混合模型，最近在 我们的工作是在多个场景分割线索中进行概括（Qiu，2013）。我们将用这个模型来测试 反映局部抑制的项是否在所有IPD中被选择性地减少，以及项的强度是否 表示长距离调制与幻视的频率相关。