Mechanisms of visual learning in cortical blindness

描述（由申请人提供）：成人初级视皮层（V1）损伤导致双眼视野相同部分的有意识视力丧失（皮质盲- CB）。这种在老年人中越来越常见的永久性残疾原因，成年人仍然被认为是不可治愈的。我们的长期目标是为理解永久性视皮层损伤后的视觉恢复定义一个新的范式。我们的目标是表征的属性和信号处理机制，使视觉再学习和恢复CB。了解哪些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，以及特定个体可以获得的恢复视力的质量和形式。我们将满足我们的目的和目标，通过测试的主要假设，即V1损伤后，训练诱导的再学习在CB领域取决于其启动的运动处理。这是基于我们的初步研究结果，CB领域的运动训练转移到静态的方向歧视，通常不能感知盲视。然而，在没有初始运动训练的情况下，这些静态辨别不能被重新学习。虽然训练可以通过各种机制起作用，但我们的初步研究结果提出了以下替代方案，在这里进行测试：1）训练刺激运动处理复合体hMT+更有效地处理来自CB场的视觉信息，包括静态方向辨别所需的信息，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的部分）和它们预先存在的处理能力，或3）训练改变来自hMT+/其它区域的信息的读出。目标1将使用视觉心理物理学来检验静态方向再学习依赖于运动路径中的学习的假设，并测量训练方向/方向的学习特异性。目标2将使用感知模板模型（PTM）和空间抑制的心理物理测试来测试CB场中的再学习通过以下方式发生的假设：1）基本方向或方向通道的调谐变化，可能通过这些通道内的空间抑制变化，或2）训练改善这些通道的读出。目标3将使用功能性MRI（fMRI）来测量与CB场中再学习相关的功能解剖学变化。我们将测试以下假设：视觉训练：1）改变仅hMT+或hMT+和其他视觉区域（V1、V2、V3、V4、V01）两者中的盲场的视网膜定位表征; 2）增加仅hMT+或hMT+和V1、V2、V3、V4、V01两者中的方向和/或定向特异性;或3）以上都没有。我们的研究结果将提供关键信息的大脑通路和信号处理机制刺激的训练，以唤起视觉再学习CB领域。这一知识在理论上是必不可少的，以更好地了解受损的成人视觉系统的可塑性的类型和程度，并改善我们的治疗策略，为人类遭受永久性视觉皮层损伤引起的残疾。

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.