Mechanisms of visual learning in cortical blindness

描述(由申请人提供)：成人初级视觉皮质(V1)的损伤会导致双眼同一视野部分的有意识视力丧失(皮质盲-CB)。这种越来越常见的导致老年人永久性残疾的原因仍然被认为是无法治疗的。我们的长期目标是定义一种新的范式来理解永久性视皮层损伤后的视觉恢复。我们的目标是表征CB的特性和信号处理机制，使其能够在CB中进行视觉再学习和恢复。了解什么机制和大脑通路调节恢复，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。我们将通过检验基本假设来达到我们的目的和目的，即在V1损伤后，训练诱导的CB区域的再学习依赖于运动加工来启动。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的方向辨别，通常用盲人看不到。然而，如果没有最初的动作训练，这些静态辨别就不能重新学习。虽然训练可以通过各种机制发挥作用，但我们的初步发现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+，以更有效地处理CB视野中的视觉信息，包括静态方位辨别所需的视觉信息；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的部分)及其预先存在的处理能力，或3)训练改变来自HMT+/其他区域的信息读出。目标1将使用视觉心理物理学来检验静态定向再学习依赖于运动路径中的学习的假设，并测量对训练方向/定向的学习的特异性。目标2将使用知觉模板模型(PTM)和空间抑制的心理物理测试来检验这一假说，即CB视野中的再学习是通过1)基本方位或方向通道的调谐改变，可能是通过改变这些通道内的空间抑制来发生的，或者2)训练改善了这些通道的读出。AIM 3将使用功能磁共振(FMRI)来测量与CB领域的再学习相关的功能解剖的变化。我们将检验视觉训练的假设：1)仅在HMT+或在HMT+和其他视觉区域(V1、V2、V3、V4、V01)中改变盲区的视网膜视觉表征；2)仅在HMT+或在HMT+和V1、V2、V3、V4、V01或3)增加方向和/或方向特异性。我们的结果将提供有关大脑通路和信号处理机制的关键信息，这些机制由训练刺激，以唤起CB领域的视觉再学习。从理论上讲，这些知识对于更好地了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的残疾患者的治疗策略是必不可少的。

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.