Functional recovery following motor cortex lesions in non-human primates: experimental implications for human stroke patients.
Functional recovery following motor cortex lesions in non-human primates: experimental implications for human stroke patients.
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DOI：
10.1142/s0219635211002737
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发表时间：
2011-09
影响因子：
1.8
通讯作者：
Morecraft RJ
中科院分区：
文献类型：
--
作者：
Darling WG;Pizzimenti MA;Morecraft RJ
本文综述了非人灵长类动物大脑皮层运动区损伤后对侧精细手运动功能恢复的经典研究和当代研究。从经典文献和当代研究的结果表明，皮层运动区的病变诱导轻瘫最初，但随后由显着的恢复精细的手/手指运动功能，这取决于病变的大小和病变后的训练。事实上，在最近的工作中，已经观察到与抓握和操纵小物体相关的精细手指功能的大量量化，非常有利的恢复是可能的，最小限度地强制使用对侧肢体。对恢复机制的研究表明，在初级运动皮层（M1）的数字区域的小损伤后，数字运动表征扩展到M1的区域，这些区域在损伤前不产生数字运动。然而，在较大的病变涉及手肘，腕和手指领域的M1，没有这样的扩展的运动代表观察，这表明恢复是由于其他皮质或皮质下区域接管控制手/手指运动。最近，我们发现，一个可能的机制，恢复损伤后的手臂地区的M1和外侧运动前皮质是增强皮质脊髓的预测，从位于内侧的辅助运动区（M2）的脊髓板层包含的神经元已经失去了大量的输入从外侧运动区，并发挥了关键作用，达到和数字运动。由于人类中风和脑损伤患者显示变量，通常较差，恢复的手运动功能比非人灵长类动物运动皮层损伤后，我们的结论与讨论的影响，这项工作的进一步实验，以改善恢复的手功能在人类中风患者。
This review discusses selected classical works and contemporary research on recovery of contralesional fine hand motor function following lesions to motor areas of the cerebral cortex in non-human primates. Findings from both the classical literature and contemporary studies show that lesions of cortical motor areas induce paresis initially, but are followed by remarkable recovery of fine hand/digit motor function that depends on lesion size and post-lesion training. Indeed, in recent work where considerable quantification of fine digit function associated with grasping and manipulating small objects has been observed, very favorable recovery is possible with minimal forced use of the contralesional limb. Studies of the mechanisms underlying recovery have shown that following small lesions of the digit areas of primary motor cortex (M1), there is expansion of the digit motor representations into areas of M1 that did not produce digit movements prior to the lesion. However, after larger lesions involving the elbow, wrist and digit areas of M1, no such expansion of the motor representation was observed, suggesting that recovery was due to other cortical or subcortical areas taking over control of hand/digit movements. Recently, we showed that one possible mechanism of recovery after lesion to the arm areas of M1 and lateral premotor cortex is enhancement of corticospinal projections from the medially located supplementary motor area (M2) to spinal cord laminae containing neurons which have lost substantial input from the lateral motor areas and play a critical role in reaching and digit movements. Because human stroke and brain injury patients show variable, and usually poorer, recovery of hand motor function than that of nonhuman primates after motor cortex damage, we conclude with a discussion of implications of this work for further experimentation to improve recovery of hand function in human stroke patients.