Learning and plasticity in the human brain

本研究的主要目标是i）确定神经系统损伤或功能障碍引起的大脑处理变化，ii）了解大脑可塑性如何促成这些变化，以及iii）确定学习如何改善这些变化的负面后果。在过去的一年里，我们继续主要关注大脑特定区域（包括视觉和躯体感觉皮层）失去输入后的可塑性。 1.视觉输入的损失。黄斑变性患者由于视网膜损伤而丧失中心视力。但是，大脑中专门处理中央视觉刺激的部分会发生什么呢？利用功能磁共振成像，我们之前已经证明，大脑中被剥夺输入的部分开始对视野其他区域的视觉刺激做出反应，就好像它们正在承担新的功能。我们把这称为视觉加工的重组。我们进一步证明，这种重组依赖于中央视觉的完全丧失，并不特定于黄斑变性患者用于固定的视网膜部分（通常称为首选视网膜位点，或PRL），并可能导致感知失真。我们目前正在研究黄斑变性视力丧失对皮质厚度的影响。据报道，在一些发育性视觉障碍中，皮质比健康对照参与者薄，但尚不清楚这种结构变化是否也发生在成年期视力丧失时。 2.失去躯体感觉输入。截肢后，超过90%的人报告他们失去的肢体有幻肢感，通常是疼痛感（幻肢痛或PLP）。目前的一种理论认为，PLP是皮层重组的直接结果，是适应不良可塑性的一个例子。镜子疗法已被用作PLP的治疗。在这种治疗过程中，患者在看镜子的同时移动他们完整的肢体，使其看起来好像他们缺失的肢体在移动。我们目前正在研究截肢的神经后果以及镜像治疗对大脑活动的影响。我们继续招募单侧截肢者，并在四周内用功能磁共振成像监测大脑活动，同时截肢者接受镜像治疗。我们正试图确定PLP的存在是否与躯体感觉和运动皮层的皮层重组相关（类似于我们在黄斑变性参与者中观察到的），以及镜像疗法是否通过减少皮层重组的程度而起作用。 确定成人皮质可塑性的性质、程度和后果，为神经系统损伤或功能障碍后的康复性脑治疗提供了重要的见解。

The primary goals of this research are i) to establish the changes in brain processing arising from nervous system damage or dysfunction, ii) to understand how brain plasticity contributes to these changes, and iii) to determine how learning may ameliorate the negative consequences of such changes. Over the past year we have continued to focus primarily on plasticity following the loss of input to particular regions of the brain, including visual and somatosensory cortex. i) Loss of visual input. People with macular degeneration lose central vision due to retinal damage. But what happens to the parts of the brain that are specifically involved in processing central visual stimuli? Using fMRI, we have previously shown that the parts of the brain deprived of input start to respond to visual stimuli in other regions of the visual field, as if they are taking on new function. We have referred to this as reorganization of visual processing. We have further demonstrated that such reorganization is dependent on complete loss of central vision, is not specific to the part of the retina used for fixation in people with macular degeneration (often referred to as the Preferred Retinal Locus, or PRL), and may lead to perceptual distortions. We are currently investigating the impact of vision loss in macular degeneration on cortical thickness. In some developmental visual disorders, the cortex has been reported to be thinner than in healthy control participants, but it is unknown whether such structural changes also occur when the vision loss happens in adulthood. ii) Loss of somatosensory input. Following limb amputation, over 90% of people report phantom sensations in their missing limb, often painful sensations (Phantom Limb Pain, or PLP). One current theory suggests that PLP is a direct result of cortical reorganization, an example of maladaptive plasticity. Mirror therapy has been used as a treatment for PLP. During this therapy, patients move their intact limb while looking in a mirror, making it seem as if their missing limb is moving. We are currently investigating the neural consequences of amputation and the impact of mirror therapy on brain activity over time. We are continuing to recruit unilateral limb amputees and monitoring brain activity with fMRI over a period of four weeks while the amputees undergo mirror therapy. We are trying to establish whether the presence of PLP correlates with cortical reorganization in the somatosensory and motor cortex (similar to that observed in our participants with macular degeneration) and whether the mirror therapy works by reducing the extent of cortical reorganization. Establishing the nature, degree and consequences of plasticity in the adult cortex provides important insights into the potential for rehabilitative brain therapies following injury or dysfunction in the nervous system.