Frontal and frontoparietal injury differentially affect the ipsilateral corticospinal projection from the nonlesioned hemisphere in monkey (Macaca mulatta).
Frontal and frontoparietal injury differentially affect the ipsilateral corticospinal projection from the nonlesioned hemisphere in monkey (Macaca mulatta).
复制标题
DOI：
10.1002/cne.23861
复制
发表时间：
2016-02-01
期刊：
影响因子：
--
通讯作者：
Darling WG
中科院分区：
文献类型：
--
作者：
Morecraft RJ;Ge J;Stilwell-Morecraft KS;McNeal DW;Hynes SM;Pizzimenti MA;Rotella DL;Darling WG
上肢偏瘫是单侧皮质卒中的常见后果。了解未受影响的大脑半球在运动恢复过程中的作用，在一定程度上是由于同侧皮质脊髓投射的存在。我们研究了从孤立性额叶损伤和孤立性额顶叶损伤自发长期恢复后，从对侧初级运动皮层（cM 1）手/臂区到脊髓水平C5-T1的同侧皮质脊髓投射（iCSP）的神经可塑性反应。高分辨率道跟踪，体视学和行为的方法进行了应用。与对照组相比，从额叶运动损伤中恢复导致cM 1的iCSP中末端标记的扣结数量增加。增加发生在第八层和相邻的腹侧部门的第七层，这是参与轴向/近端肢体感觉运动处理。较大的额叶病变与更多的终端扣比较小的额叶病变。与此相反，额顶叶损伤阻止了这种反应，因为总的bouton数是类似的控制，表明中断的体感输入到一个半球有抑制作用的iCSP从非病变半球。然而，与对照组相比，升高的终扣数发生在第八层，在第七层终扣标记的费用。在两个额顶叶病变的病例中，第九层扣结也升高，伴有广泛的皮质损伤。由于第八层和第九层共同港轴向，近端和远端运动神经元，治疗干预针对同侧皮质脊髓连接从cM 1可能会促进近端，并可能远端，上肢运动功能恢复后，额叶和额顶叶损伤。额叶运动损伤后，在第VIII层和第VII层周围亚区发现对侧病灶M1的同侧皮质脊髓投射增生（上图），可能支持轴向/近端上肢运动恢复。这种整体反应在额顶叶损伤后被阻断，但向第VIII层的投射仍然升高（下图）。
Upper extremity hemiplegia is a common consequence of unilateral cortical stroke. Understanding the role of the unaffected cerebral hemisphere in the motor recovery process has been encouraged, in part, by the presence of ipsilateral corticospinal projections. We examined the neuroplastic response of the ipsilateral corticospinal projection (iCSP) from the contralesional primary motor cortex (cM1) hand/arm area to spinal levels C5-T1 after spontaneous long-term recovery from isolated frontal lobe injury and isolated frontoparietal injury. High-resolution tract tracing, stereological, and behavioral methodologies were applied. Recovery from frontal motor injury resulted in enhanced numbers of terminal labeled boutons in the iCSP from cM1 compared to controls. Increases occurred in lamina VIII and the adjacent ventral sectors of lamina VII, which are involved in axial/proximal limb sensorimotor processing. Larger frontal lobe lesions were associated with greater numbers of terminal boutons than smaller frontal lobe lesions. In contrast, frontoparietal injury blocked this response, as total bouton number was similar to controls, demonstrating that disruption of somatosensory input to one hemisphere has a suppressive effect on the iCSP from the non-lesioned hemisphere. However, compared to controls, elevated bouton numbers occurred in lamina VIII, at the expense of lamina VII bouton labeling. Lamina IX boutons were also elevated in two frontoparietal lesion cases with extensive cortical injury. Since lamina VIII and IX collectively harbor axial, proximal, and distal motoneurons, therapeutic intervention targeting the ipsilateral corticospinal linkage from cM1 may promote proximal, and possibly distal, upper limb motor recovery following frontal and frontoparietal injury. Proliferation of the ipsilateral corticospinal projection from contralesional M1 was found in lamina VIII and surrounding subsectors of lamina VII following frontal motor injury (top), potentially supporting axial/proximal upper limb motor recovery. This overall response was blocked following frontoparietal injury, but the projection to lamina VIII remained elevated (bottom).