弱视的神经可塑性

B. Thompson
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引用次数: 2

摘要

在生命早期,大脑有很大的变化能力,通常被称为神经可塑性。在神经可塑性增强的早期“关键”或“敏感期”,大脑的视觉输入受到干扰,会引起神经系统的结构和功能变化,并导致弱视,这是一种与大脑感知区域异常发育有关的感觉障碍。弱视损害了广泛的视觉、多感觉和运动功能,从弱视中恢复需要大脑内视觉信息处理的实质性改变。因此,弱视不仅是由视觉体验和神经可塑性增强的相互作用引起的,而且弱视的恢复也需要大脑内发生显著的神经可塑性变化。许多基于证据的治疗方法可用于弱视儿童,他们的大脑仍在快速发育,具有相应的高水平神经可塑性。然而,患有弱视的成年人往往没有得到治疗,因为他们认为成年人的大脑不再具有足够的神经可塑性来重新学习如何处理视觉信息。在21世纪初,很明显这个想法是不正确的。许多可以增强成熟视觉皮层神经可塑性的干预措施已经在弱视动物模型中被确定,现在正被转化为人类研究。其他有希望的增强视觉皮层神经可塑性的技术已经从弱视成人的研究中出现。可以改善成人弱视视力的干预措施包括屈光矫正、配戴弱视眼(反向配戴)、单眼和双眼知觉学习、非侵入性脑刺激、全身药物和锻炼。该领域研究的下一个重要阶段将是进行完全对照的随机临床试验,以评估哪些干预措施(如果有的话)可以转化为成年弱视的主流治疗方法。
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Neural Plasticity in Amblyopia
Early in life, the brain has a substantial capacity for change, often referred to as neuroplasticity. Disrupted visual input to the brain during an early “critical” or “sensitive period” of heightened neuroplasticity induces structural and functional changes within neural systems and causes amblyopia, a sensory disorder associated with abnormal development of the brain areas involved in perception. Amblyopia impairs a broad range of visual, multisensory, and motor functions, and recovery from amblyopia requires a substantial change in visual information processing within the brain. Therefore, not only is amblyopia caused by an interaction between visual experience and heightened neuroplasticity, recovery from amblyopia also requires significant neuroplastic change within the brain. A number of evidence-based treatments are available for young children with amblyopia whose brains are still rapidly developing and have a correspondingly high level of neuroplasticity. However, adults with amblyopia are often left untreated because of the idea that the adult brain no longer has sufficient neuroplasticity to relearn how to process visual information. In the early 21st century, it became clear that this idea was not correct. A number of interventions that can enhance neuroplasticity in the mature visual cortex have been identified using animal models of amblyopia and are now being translated into human studies. Other promising techniques for enhancing visual cortex neuroplasticity have emerged from studies of adult humans with amblyopia. Examples of interventions that may improve vision in adult amblyopia include refractive correction, patching of the amblyopic eye (reverse patching), monocular and binocular perceptual learning, noninvasive brain stimulation, systemic drugs, and exercise. The next important stage of research within this field will be to conduct fully controlled randomized clinical trials to assess which, if any, of these interventions can be translated into a mainstream treatment for amblyopia in adulthood.
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