Sasaki K, Gemba H
Institute for Brain Research, Faculty of Medicine, Kyoto University, Japan.
Acta Neurochir Suppl (Wien). 1987;41:18-28. doi: 10.1007/978-3-7091-8945-0_4.
Processes of motor learning and of compensation after localized brain dysfunction were studied in the monkey tasked with conditioned (visually-initiated, reaction-time) hand movements. Field potentials in various cortical areas of the cerebral hemisphere were recorded successively for many months with electrodes implanted on the surface and in the depth of the cortex. The potentials associated with the conditioned movement were found to change during processes of learning the movement and during courses of degradation as well as recovery after the brain dysfunction. Motor learning of the reaction-time movement can be categorized into "recognition" and "skill" learnings. The former is the process for associating the visual stimulus with the movement and accompanied mainly by increasing activities of prefrontal, premotor and prestriate cortices. The latter is attaining better performances in executing the movement, particularly with shorter and more fixed reaction time, and is accompanied by recruitment of the cerebro-cerebellar interaction. The conditioned movements which had been well established were experimentally disturbed by transient, local cooling of different cortical areas or by cerebellar hemispherectomy. Three possible mechanisms of compensation are proposed as follow: 1. Substitution: Compensation occurring immediately through substitutional neuronal circuits. On transient cooling of the forelimb motor cortex, the somatosensory cortex became predominant in motor function and replaced the disabled motor cortex in executing the reaction-time movement, although activity was weak and slow (paretic but not paralytic). Resection of the cerebellar hemisphere also induced the compensatory motor function of the somatosensory cortex so that the movement could be performed although it was weak, slow and clumsy. 2. Relearning: Compensation by relearning through normally unused neuronal circuits. Prolonged and variable reaction times after cerebellar hemispherectomy persisted when the operation included both dentate and interpositus nuclei but recovered within about three weeks when the interpositus nucleus was preserved. It is suggested that the information processing for the well accomplished reaction-time movement is mainly mediated by the cerebro-cerebellar neuronal circuit including the dentate nucleus but is gradually relearned through the normally unused circuits involving the interpositus nucleus after the dentate nucleus lesion. 3. Rebuilding: Compensation by rebuilt neuronal circuits, e.g., by sprouting and/or regeneration (see S. Kawaguchi in this book).
在以条件性(视觉引发、反应时)手部运动为任务的猴子身上,研究了运动学习和局部脑功能障碍后的代偿过程。通过将电极植入大脑皮层表面和深部,连续数月记录大脑半球各个皮层区域的场电位。发现与条件性运动相关的电位在运动学习过程中以及脑功能障碍后的退化和恢复过程中都会发生变化。反应时运动的运动学习可分为“认知”学习和“技能”学习。前者是将视觉刺激与运动联系起来的过程,主要伴随着前额叶、运动前区和纹前皮层活动的增加。后者是在执行运动时获得更好的表现,特别是反应时更短且更稳定,并伴随着大脑-小脑相互作用的增强。通过对不同皮层区域进行短暂局部冷却或小脑半球切除术,对已建立良好的条件性运动进行实验性干扰。提出了三种可能的代偿机制如下:1. 替代:通过替代神经元回路立即发生代偿。在前肢运动皮层短暂冷却时,体感皮层在运动功能中占主导地位,并在执行反应时运动中取代了受损的运动皮层,尽管活动较弱且缓慢(轻瘫但非瘫痪)。切除小脑半球也会诱导体感皮层的代偿运动功能,从而使运动能够进行,尽管运动较弱、缓慢且笨拙。2. 重新学习:通过通常未使用的神经元回路重新学习进行代偿。当手术包括齿状核和间位核时,小脑半球切除术后反应时延长且变化不定,但当保留间位核时,约三周内恢复。这表明,对于完成良好的反应时运动,信息处理主要由包括齿状核在内的大脑-小脑神经元回路介导,但在齿状核损伤后,逐渐通过涉及间位核的通常未使用的回路重新学习。3. 重建:通过重建神经元回路进行代偿,例如通过发芽和/或再生(见本书中的S. Kawaguchi)。