Cognitive routes to the rehabilitation of unilateral neglect
Cognitive routes to the rehabilitation of unilateral neglect
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单方面忽视康复的认知途径
DOI：
10.1093/acprof:oso/9780198508335.003.0026
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发表时间：
2002
影响因子：
0.4
通讯作者：
T. Manly
中科院分区：
文献类型：
--
作者：
I. Robertson;T. Manly
长期以来，认知神经科学一直致力于为脑损伤的有效认知康复发展带来实实在在的好处。在本章中，我们将论证，在单方面忽视领域，这一目标已经部分实现。此外，单侧忽视的认知康复研究也促进了认知神经科学的理论发展，产生了独特的共生关系，我们希望这将成为认知功能和功能障碍的其他领域的一个例子。为了本章的目的，我们将认知康复定义为“系统地使用指导和结构化经验来操纵认知系统的功能，例如提高特定领域认知处理的质量和/或数量”。（Robertson 1999）。这一定义受到了过去十年研究文献的影响，例如，长期以来关于大脑的一个核心假设--新的细胞体不能在成年期出现--被戏剧性地推翻了。最近对人类和动物的数据表明，海马体中确实可以产生新的细胞（Eriksson et al. 1998）。更重要的是，这一过程部分是经验依赖性的，与贫困环境相比，在丰富环境中饲养的动物在海马体中显示出更多的细胞发生（Gould et al. 1999）。这一发现紧随着过去十年的另一项革命性发现--证明成年人的大脑可以在神经回路中显示出巨大的经验依赖性变化，包括树突和轴突发芽（Recanzone et al. 1993）。有充分的理由相信，在受损的大脑中也会发生类似的可塑性变化（Seitz et al. 1995），并且这些变化在一定程度上介导了脑损伤后功能的恢复。因此，康复现在可以把注意力转向通过适当的计划经验直接改变神经回路的雄心勃勃的目标。这种对神经回路的直接影响已经在灵长类动物中得到证实（Nudo等人，1996年）。虽然一些康复方面的先驱研究人员认为，在某些情况下，康复可能会对神经系统产生直接影响，（Bach-y-Rita 1989），普遍的观点是，脑损伤后的康复通过促进Luria（1963）所称的“功能重组”而产生效果，为了以不同的方式实现受损的行为目标，幸存的未受损脑回路的补偿性重组-这种机制确实是行为恢复的基础（Robertson and Murre 1999）。从脑损伤中恢复的第三种方式是通过健康的竞争者回路解除对受损网络的抑制（Robertson和Murre 1999）。这可以通过抑制抑制竞争或通过增强受损网络中回路的激活来实现。
Cognitive neuroscience has long held out the promise of yielding tangible benefits to the development of effective cognitive rehabilitation of brain damage. In this chapter we will argue that in the field of unilateral neglect, this goal has been partly achieved. Furthermore, cognitive rehabilitation research in unilateral neglect has also contributed to theoretical developments in cognitive neuroscience, yielding a unique symbiosis which we hope will serve as an example for other domains of cognitive function and dysfunction. For the purposes of this chapter, we will define cognitive rehabilitation as ‘the systematic use of instruction and structured experience to manipulate the functioning of cognitive systems such as to improve the quality and/or quantity of cognitive processing in a particular domain’(Robertson 1999).This definition has been influenced by the research literature of the last decade which has seen, for instance, the dramatic disconfirmation of a long-held central assumption about the brain—that new cell bodies cannot emerge in adulthood. Recent data for both humans and animals have shown that new cells can indeed be produced in the hippocampus (Eriksson et al. 1998). What is more, this process is partly experience dependent—animals kept in enriched compared with impoverished environments show more cell genesis in the hippocampus (Gould et al. 1999). This finding follows close on the heels of another revolutionary discovery of the last decade—the demonstration that the adult brain can show large experience-dependent changes in neural circuits, including dendritic and axonal sprouting (Recanzone et al. 1993). There is every reason to believe that parallel plastic changes also occur in the damaged brain (Seitz et al. 1995), and that such changes mediate in part recovery of function after brain damage. Therefore rehabilitation can now turn its attention to the ambitious goal of directly altering neural circuitry through appropriately planned experience. Such direct effects on neural circuits have already been demonstrated in primates (Nudo et al. 1996). While some pioneering researchers on rehabilitation have argued that rehabilitation may under certain circumstances have direct neural effects (Bach-y-Rita 1989), the prevailing view has been that rehabilitation following brain damage had its effects by fostering what Luria (1963) termed ‘functional reorganization’—the compensatory reorganization of surviving undamaged brain circuits in order to achieve the impaired behavioral goals in a different way—and such mechanisms do indeed underpin much behavioral recovery (Robertson and Murre 1999). A third way in which recovery from brain damage can take place is through the lifting of inhibition over damaged networks by healthy competitor circuits (Robertson and Murre 1999). This can take place either by damping down the inhibitory competition, or by boosting the activation in circuits in the lesioned network.