Byl N N, Merzenich M M, Jenkins W M
Coleman Laboratory, Department of Otolaryngology, University of California at San Francisco 94143-0732, USA.
Neurology. 1996 Aug;47(2):508-20. doi: 10.1212/wnl.47.2.508.
In this study we tested a neuroplasticity/learning origins hypothesis for repetitive strain injuries (RSIs), including occupationally induced focal dystonia. Repetitive movements produced in a specific form and in an appropriate behavioral context cause a degradation of the sensory feedback information controlling fine motor movements, resulting in the "learned" genesis of RSIs. Two adult New World owl monkeys were trained at a behavioral task that required them to maintain an attended grasp on a hand grip that repetitively and rapidly (20 msec) opened and closed over short distances. The monkeys completed 300 behavioral trials per day (1,100 to 3,000 movement events) with an accuracy of 80 to 90%. A movement control disorder was recorded in both monkeys. Training was continued until the performance accuracy dropped to below 50%. We subsequently conducted an electrophysiologic mapping study of the representations of the hand within the primary somatosensory (SI) cortical zone. The hand representation in the true primary somatosensory cortical field, SI area 3b, was found to be markedly degraded in these monkeys, as characterized by (1) a dedifferentiation of cortical representations of the skin of the hand manifested by receptive fields that were 10 to 20 times larger than normal, (2) the emergence of many receptive fields that covered the entire glabrous surface of individual digits or that extended across the surfaces of two or more digits, (3) a breakdown of the normally sharply segregated area 3b representations of volar glabrous and dorsal hairy skin of the hand, and (4) a breakdown of the local shifted-overlap receptive field topography of area 3b, with many digital receptive fields overlapping the fields of neurons sampled in cortical penetrations up to more than four times farther apart than normal. Thus, rapid, repetitive, highly stereotypic movements applied in a learning context can actively degrade cortical representations of sensory information guiding fine motor hand movements. This cortical plasticity/learning-based dedifferentiation of sensory feedback information from the hand contributes to the genesis of occupationally derived repetitive strain injuries, including focal dystonia of the hand. Successful treatment of patients with RSI will plausibly require learning-based restoration of differentiated representations of sensory feedback information from the hand.
在本研究中,我们对重复性劳损(RSI),包括职业性局灶性肌张力障碍,检验了一种神经可塑性/学习起源假说。以特定形式并在适当行为背景下产生的重复性动作会导致控制精细运动的感觉反馈信息退化,从而导致RSI的“习得性”成因。对两只成年新大陆猫头鹰猴进行一项行为任务训练,要求它们在一个手柄上保持持续抓握,该手柄会在短距离内反复且快速地(20毫秒)开合。猴子每天完成300次行为试验(1100至3000次运动事件),准确率为80%至90%。两只猴子均出现了运动控制障碍。训练持续进行,直至表现准确率降至50%以下。随后,我们对初级体感(SI)皮质区内手部表征进行了电生理图谱研究。发现在这些猴子中,真正的初级体感皮质区SI区3b内的手部表征明显退化,其特征为:(1)手部皮肤皮质表征的去分化,表现为感受野比正常情况大10至20倍;(2)出现许多覆盖单个手指整个无毛表面或延伸至两个或更多手指表面的感受野;(3)手部掌侧无毛皮肤和背侧有毛皮肤在正常情况下明显分隔的3b区表征遭到破坏;(4)3b区局部移位重叠感受野地形图遭到破坏,许多手指感受野与皮质穿透采样的神经元感受野重叠,其间距比正常情况远四倍以上。因此,在学习背景下施加的快速、重复、高度刻板的动作会主动降解指导手部精细运动的感觉信息的皮质表征。这种基于皮质可塑性/学习的手部感觉反馈信息去分化促成了职业性重复性劳损的成因,包括手部局灶性肌张力障碍。对RSI患者的成功治疗可能需要基于学习来恢复来自手部的感觉反馈信息的分化表征。