Institute of Medical Psychology, Medical Faculty, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
Prog Brain Res. 2011;192:199-262. doi: 10.1016/B978-0-444-53355-5.00013-0.
Vision loss after retinal or cerebral visual injury (CVI) was long considered to be irreversible. However, there is considerable potential for vision restoration and recovery even in adulthood. Here, we propose the "residual vision activation theory" of how visual functions can be reactivated and restored. CVI is usually not complete, but some structures are typically spared by the damage. They include (i) areas of partial damage at the visual field border, (ii) "islands" of surviving tissue inside the blind field, (iii) extrastriate pathways unaffected by the damage, and (iv) downstream, higher-level neuronal networks. However, residual structures have a triple handicap to be fully functional: (i) fewer neurons, (ii) lack of sufficient attentional resources because of the dominant intact hemisphere caused by excitation/inhibition dysbalance, and (iii) disturbance in their temporal processing. Because of this resulting activation loss, residual structures are unable to contribute much to everyday vision, and their "non-use" further impairs synaptic strength. However, residual structures can be reactivated by engaging them in repetitive stimulation by different means: (i) visual experience, (ii) visual training, or (iii) noninvasive electrical brain current stimulation. These methods lead to strengthening of synaptic transmission and synchronization of partially damaged structures (within-systems plasticity) and downstream neuronal networks (network plasticity). Just as in normal perceptual learning, synaptic plasticity can improve vision and lead to vision restoration. This can be induced at any time after the lesion, at all ages and in all types of visual field impairments after retinal or brain damage (stroke, neurotrauma, glaucoma, amblyopia, age-related macular degeneration). If and to what extent vision restoration can be achieved is a function of the amount of residual tissue and its activation state. However, sustained improvements require repetitive stimulation which, depending on the method, may take days (noninvasive brain stimulation) or months (behavioral training). By becoming again engaged in everyday vision, (re)activation of areas of residual vision outlasts the stimulation period, thus contributing to lasting vision restoration and improvements in quality of life.
视网膜或脑视觉损伤（CVI）后的视力丧失长期以来被认为是不可逆转的。然而，即使在成年后，视力恢复和恢复也有相当大的潜力。在这里，我们提出了“残余视觉激活理论”，说明视觉功能如何被重新激活和恢复。CVI 通常不是完全的，但损伤通常会保留一些结构。它们包括（i）视野边界的部分损伤区域，（ii）盲区内幸存组织的“岛屿”，（iii）不受损伤影响的外纹状途径，以及（iv）下游的高级神经元网络。然而，残余结构有三重障碍使其完全发挥功能：（i）神经元较少，（ii）由于兴奋/抑制失衡导致主导的完整半球，缺乏足够的注意力资源，以及（iii）其时间处理受到干扰。由于这种激活损失，残余结构无法为日常视力做出很大贡献，并且它们的“不使用”进一步削弱了突触强度。然而，残余结构可以通过不同的方式（i）视觉体验、（ii）视觉训练或（iii）非侵入性脑电流刺激来重新激活。这些方法导致突触传递的增强和部分损伤结构的同步（内系统可塑性）和下游神经元网络（网络可塑性）。就像在正常的知觉学习中一样，突触可塑性可以改善视力并导致视力恢复。这种情况可以在损伤后任何时间、任何年龄和所有类型的视网膜或脑损伤（中风、神经创伤、青光眼、弱视、年龄相关性黄斑变性）后的视野损伤中诱导。视觉恢复的程度和程度取决于残余组织的数量及其激活状态。然而，持续的改善需要重复刺激，这取决于方法，可能需要数天（非侵入性脑刺激）或数月（行为训练）。通过再次参与日常视觉，残余视觉区域的（重新）激活持续时间超过刺激期，从而有助于持久的视力恢复和生活质量的提高。
