Corticospinal tract development and its plasticity after perinatal injury
Corticospinal tract development and its plasticity after perinatal injury
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DOI：
10.1016/j.neubiorev.2007.05.011
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发表时间：
2007-01-01
影响因子：
8.2
通讯作者：
Eyre, J. A.
中科院分区：
文献类型：
--
作者：
Eyre, J. A.
皮质脊髓束的起源和终止的最终模式是在发育过程中通过轴突的投射和撤回之间的平衡形成的。在动物中，发育期间对感觉运动皮质的单侧抑制会导致该皮质的对侧投射稀疏，并保留来自更活跃皮质的更多同侧投射。类似地，在患有偏瘫型脑瘫的受试者中，如果受损运动皮层的经颅磁刺激（TMS）未能引起麻痹上肢的反应，则未受损的同侧运动皮层的TMS引起异常大且短的反应。而不是代表一个“修复可塑性的损伤”，这篇评论提出的证据表明，增加同侧的预测，从非梗死运动皮层产生的扰动正在进行的发展过程中，从而减少活动，在受损的半肢，导致其存活的对侧皮质脊髓投射的撤回增加，因为它们的终末已被未受损的更活跃的同侧投射所取代大脑半球，从而增加了长期运动障碍的程度。(c)2007爱思唯尔有限公司保留所有权利。
The final pattern of the origin and termination of the corticospinal tract is shaped during development by the balance between projection and withdrawal of axons. In animals, unilateral inhibition of the sensorimotor cortex during development results in a sparse contralateral projection from this cortex and retention of a greater number of ipsilateral projections from the more active cortex. Similarly in subjects with hemiplegic cerebral palsy if transcranial magnetic stimulation (TMS) of the damaged motor cortex fails to evoke responses in the paretic upper limb, TMS of the undamaged ipsilateral motor cortex evokes abnormally large and short-onset responses. Rather than representing a "reparative plasticity in response to injury", this review presents evidence that increased ipsilateral projections from the non-infarcted motor cortex arise from perturbation of ongoing developmental processes, whereby reduced activity in the damaged hemipshere, leads to increased withdrawal of its surviving contralateral corticospinal projections because their terminals have been displaced by the more active ipsilateral projections of the undamaged hemisphere and thereby adding to the degree of long-term motor impairment. (c) 2007 Elsevier Ltd. All rights reserved.