Mechanisms of visual learning in cortical blindness

描述（由申请人提供）：成人初级视觉皮层（V1）的损伤导致双眼视野同一部分的有意识视力丧失（皮质性失明- CB）。这种导致老年人终身残疾的日益常见的原因仍被认为是无法治愈的。我们的长期目标是定义一种理解永久性视觉皮层损伤后视力恢复的新范式。我们的目标是表征在CB中实现视觉再学习和恢复的特性和信号处理机制。了解什么机制和大脑通路介导恢复将使我们能够预测视力可以恢复的程度，以及在特定个体中可以获得的恢复视力的质量和方式。我们将通过验证V1损伤后训练诱导的再学习依赖于运动处理启动的主要假设来实现我们的目标。这是基于我们的初步发现，在CB领域的运动训练转移到静态方向的区别，而不是在盲视正常感知。然而，如果没有最初的运动训练，这些静态识别就不能被重新学习。虽然培训可以通过多种机制发挥作用，但我们的初步研究结果提出了以下可供测试的替代方案：1)训练刺激运动处理复合物hMT+更有效地处理来自CB场的视觉信息，包括静态方向识别所需的视觉信息；2)训练刺激运动通路重新激活其他视觉区域（包括V1， V2, V3, V4， V01部分）及其原有的处理能力；或3)训练改变hMT+/其他区域的信息读出。目的1将使用视觉心理物理学来验证静态定向再学习依赖于运动路径学习的假设，并测量训练方向/定向学习的特异性。目的2将使用感知模板模型（PTM）和空间抑制的心理物理测试来验证以下假设：CB领域的再学习发生在1)基本方向或方向通道的调谐变化，可能是通过这些通道内空间抑制的变化，或者2)训练提高了这些通道的读出。目的3将使用功能磁共振成像（fMRI）来测量与CB领域再学习相关的功能解剖学变化。我们将检验视觉训练的假设：1)改变盲区在hMT+或hMT+和其他视觉区域（V1, V2, V3, V4, V01）的视网膜定位表征；2)仅在hMT+中或在hMT+和V1、V2、V3、V4、V01中均增加方向和/或方向特异性，或3)以上均不增加。我们的研究结果将提供有关脑通路和信号处理机制的重要信息，这些通路和信号处理机制是由训练刺激来唤起视觉再学习的。从理论上讲，这一知识对于更好地理解受损成人视觉系统的可塑性类型和程度，以及改进我们对因永久性视觉皮质损伤而导致残疾的人类的治疗策略至关重要。

DESCRIPTION (provided by applicant): Damage to the adult primary visual cortex (V1) causes a loss of conscious vision over the same part of the visual field in both eyes (cortical blindness - CB). This increasingly common cause of permanent disability in older, adult humans is still considered untreatable. Our long-term objective is to define a new paradigm for understanding visual recovery after permanent visual cortex damage. Our goal is to characterize the properties of and signal processing mechanisms that enable visual relearning and recovery in CB. Knowing what mechanisms and brain pathways mediate recovery will allow us to predict the extent to which vision can be recovered, as well as the quality and modality of recovered vision that can be attained in a given individual. We will meet our objective and goal by testing the primary hypothesis that after V1 damage, training-induced relearning in CB fields depends on motion processing for its initiation. This is based on our preliminary findings that motion training in CB fields transfers to static orientation discriminations not normally perceivable in blindsight. However, without the initial motion training, these static discriminations cannot be relearned. While training could work via a variety of mechanisms, our preliminary findings suggest the following alternatives, to be tested here: 1) training stimulates the motion processing complex hMT+ to more effectively process visual information from CB fields, including that needed for static orientation discriminations, 2) training stimulates the motion pathway to reactivate other visual areas (incl. parts of V1, V2, V3, V4, V01) and their pre-existing processing abilities, or 3) training alters readout of information from hMT+/other areas. Aim 1 will use visual psychophysics to test the hypothesis that static orientation relearning depends on learning in the motion pathway, and to measure specificity of learning for trained directions/orientations. Aim 2 will use the perceptual template model (PTM) and psychophysical tests of spatial suppression to test the hypothesis that relearning in CB fields occurs via 1) changes in tuning of basic orientation or direction channels, possibly via changes in spatial suppression within these channels, or 2) that training improves the readout of these channels. Aim 3 will use functional MRI (fMRI) to measure changes in functional anatomy associated with relearning in CB fields. We will test the hypothesis that visual training: 1) alters the blind field's retinotopic representation either in just hMT+ or both in hMT+ and other visual areas (V1, V2, V3, V4, V01); 2) increases direction and/or orientation specificity in just hMT+ or both in hMT+ and V1, V2, V3, V4, V01 or 3) none of the above. Our results will provide critical information about brain pathways and signal processing mechanisms stimulated by training to evoke visual relearning in CB fields. This knowledge is essential theoretically to better understand the type and degree of plasticity possible in damaged, adult visual systems, and to improve our treatment strategies for humans suffering from the disability induced by permanent visual cortical damage.